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TRANSCORTICAL SENSORY APHASIA PRODUCED BY LESIONS OF THE ANTERIOR BASAL GANGLIA AREA Atsushi Yamadori 1 , Takako Ohira 2 , Miki Seriu 2 , Jun Ogura 3 1Neurology Service Hyogo Brain and Heart Center at Himeji 2Neuropsychotogy Section Hyogo Brain and Heart Center at Himeji 3Department of Neuropsychiatry, Kobe University School of Medicine pp.261-266
Published Date 1984/3/1
DOI https://doi.org/10.11477/mf.1406205285
  • Abstract
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We reported three cases of an aphasic syndrome caused by unusual lesion distribution. Cur patients, language disorders could be summarized as trans-cortical sensory aphasia and showed following symptoms; ( 1) fluent paraphasic verbal output, ( 2 ) anomia which was not facilitated by cueing, ( 3 ) impaired comprehension of spoken language, ( 4 ) preserved capacity of repetition, ( 5 ) preser-ved ability of reading aloud with impaired comp-rehension of the written material and ( 6 ) agra-phia. In addition, all had no associated physical neurological signs such as hemiparesis or hemi-anopsia. All were right handed.

All three cases showed the similar lesion dist-ribution by computed tomographic scanning of the brain. All had low density areas in the anterior portion of the left basal ganglia including the head of the caudate nucleus, the anterior portion of the putamen, the anterior portion of the ante-rior limb of the internal capsule and the nearby white matter. Case 2 also had the small right he-misphere lesion in the white matter near the anterior portion of the lateral ventricle.

All three cases showed the similar lesion dist-ribution by computed tomographic scanning of the brain. All had low density areas in the anterior portion of the left basal ganglia including the head of the caudate nucleus, the anterior portion of the putamen, the anterior portion of the ante-rior limb of the internal capsule and the nearby white matter. Case 2 also had the small right he-misphere lesion in the white matter near the anterior portion of the lateral ventricle.

Transcortical sensory aphasia with this lesion distribution has not been reported. We attributed the causative damage to lesions of the white mat-ter and not to lesions of the basal ganglia per se. It was also speculated that fluent aphasia can be produced by the anteriorly situated white matter lesion if issuing fibers from the Broca's area were spared.

Finally a possible anatomoclinical correlation for"transcortical alexia" (preserved oral reading and impaired reading comprehension) was attempted. The symptom is probably a reflection of the fact that the posterior speech area including the angu-lar gyrus was left intact.


Copyright © 1984, 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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