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Brain and Nerve No to Shinkei Volume 45, Issue 11 （November 1993）

Brain and Nerve 脳と神経 45巻11号（1993年11月発行）

Japanese English

症例報告

大脳皮質の広範な多発脳梗塞様所見で発症した低血糖脳症—X線CTによる経時的検討 Hypoglycemic Encephalopathy Demonstrating Generalized Multiple Cortical Infarctions : Sequential CT Findings 磯野理 ¹ , 荒木重夫 ¹ , 塩田純一 ¹ , 豊田恵徳 ¹ , 杉田幸二郎 ² Osamu Isono ¹ , Shigeo Araki ¹ , Jun-ichi Shiota ¹ , Shigenori Toyota ¹ , Koujiro Sugita ² ¹汐田総合病院神経内科 ²昭和大学神経内科 ¹Department of Neurology, Ushioda General Hospital ²Department of Neurology, Showa University School of Medicine キーワード： hypoglycemic encephalopathy , multi-infarct like change , cerebral cortex , anoxic encephalopathy , CT scans of the brain Keyword: hypoglycemic encephalopathy , multi-infarct like change , cerebral cortex , anoxic encephalopathy , CT scans of the brain pp.1061-1066

発行日 1993年11月1日 Published Date 1993/11/1

DOI https://doi.org/10.11477/mf.1406900561

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Abstract 文献概要
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　アルコール性低血糖脳症の59歳，男性例の急性期から慢性期に至る頭部X線CTの経時的変化を追跡した。脳症発症24時間後に大脳皮質優位に広範な多発性低吸収域が出現し多発脳梗塞様所見を呈し，第4病日には低吸収域は増強して広範な瀰漫性脳浮腫と一部大脳皮質で造影増強効果がみられた。第16病日には大脳皮質の低吸収域は消失し，第23病日には大脳皮質脳回の全域に著明な造影増強効果（gyral enhance—ment）が出現し，その後急速に脳萎縮が進行した。このような特に急性期の画像上の経時的変化は低血糖脳症に特異的であり，神経病理学的に同一とされてきた無酸素脳症とは異なる病態で低血糖による脳萎縮が起こる可能性が示唆された。

A fifty-nine-year-old alcoholic man with severe hypoglycemic encephalopathy was examined using sequential CT scans of the brain (CT). Twenty-seven hours after the attack, which resulted in a comatose state, CT disclosed multiple low density areas throughout the cerebral cortex which resem-bled multiple cortical infarctions. CT obtained four days after the ictus demonstrated more prominent low density areas in the cerebal cortex, diffuse cerebral edema and partial cortical enhancement after administration of contrast medium. Sixteen days after the ictus, the multiple low density areas in the cerebral cortex disappeared. Enhanced CT on day 23 demonstrated marked gyral enhancementthroughout the cerebral cortex. Thereafter diffuse brain atrophy progressed rapidly as demonstrated by MRI on day 82 which showed extensive cortical and subcortical atrophy particularly in the fronto-parietal and parieto-occipital regions bilaterally with dilatated lateral ventricles.

Hypoglycemia and anoxia have long been thought to give rise to similar types of brain damage based on neuropathological observations. But it has recently been shown that they are quite different based on neurochemical and neurophysiological findings. Numerous previously reported autopsy cases of hypoglycemia confirm these findings which are neuropathologically similar to the multiple infarction seen in the present case.

We conclude that the acute cortical changes of the present case are specific for hypoglycemic ence-phalopathy. The findings indicate that the basic mechanisms operating in hypoglycemia and anoxia are different.