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抄録 69歳の右利き男性で,右後大脳動脈領域の梗塞により左半側空間失認をはじめ,軽度の痴呆,地誌的概念の喪失,系列言語の障害,計算障害などの多彩な神経心理学的症状を呈した1症例に,133Xeを用いたSPECTを施行した。CTでは,右後頭葉と右視床後外側部,内包後脚の一部に低吸収域が限局していたが,SPECTでは,さらに広範な領域で局所脳血流量の低下を認め,従来左半側空間失認の責任病巣とされてきた右頭頂-側頭-後頭葉接合部を含んでいた。
これまでの報告に関する文献的考察から,本症例の左半側空間失認の責任病巣として,1)右後頭葉内側面,2)右視床,3)右内包後脚,4)右頭頂-側頭-後頭葉接合部が考えられたが,SPECTの結果および臨床経過から,右頭頂-側頭-後頭葉接合部の機能低下によるものと考察した。
Left-sided unilateral spatial neglect (USN) is considered to be associated with lesions of the right parietal lobe, but has also been reported in cases with right frontal lobe lesion, right thalamic hemorrhage, right putaminal hemorrhage, right posterior internal capsule infarction, and right posterior cerebral artery (PCA) occlusion. We report a case of leftsided USN induced by the cerebral infarction in the distribution of right PCA.
A 69-year-old, right-handed man, who had had a sudden onset of left hemiparesis in August 1983, was admitted to our hospital on January 16, 1984, because of nocturnal delirium. He became alert a few days after admission, but was euphoric andsometimes irritable. Neurologic examination disclosed left homonymous hemianopsia, dysarthria, left central facial weakness, spastic left hemiparesis, hyperactive reflexes on the left with no Babinski sign, left hemisensory loss, and left thalamic pain. On neuropsychologic examination it was revealed that he had a tendency to neglect the left half of his extrapersonal space. When asked to locate cities on a blank map of Japan, he located most of them not only on the right side of the map but also incorrectly. He also had a severe acalculia. There was gradual improvement in these neuropsychologic symptoms. CT demonstrated an area of decreased density in the territory of the right PCA, posterolateral portion of the right thalamus, and the posterior limb of right internal capsule, sparing parietal and temporal lobes. Singlephoton emission computed tomography (SPECT) using the Xenon-133 inhalation method showed, however, diminished regional cerebral blood flow (rCBF) in an area larger than the area of infarction demonstrated by CT, including the right parieto-temporo-occipital junctional area, which has been considerd to be responsible for left-sided USN. The authors ascribed the patient's left-sided USN to the lesion of this area that was revealed not morphologically by CT but functionally by SPECT, although the possibility that the lesions of the medial portion of the right occipital lobe and/or subcortical lesions of such areas as the thalamus and the internal capsule more or less influenced the neuropsychologic symp-toms could not be excluded.
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