Conduction aphasia and the arcuate fasciculus: A reexamination of the Wernicke-Geschwind model

被引:138
作者
Anderson, JM
Gilmore, R
Roper, S
Crosson, B
Bauer, RM
Nadeau, S
Beversdorf, DQ
Cibula, J
Rogish, M
Kortencamp, S
Hughes, JD
Rothi, LJG
Heilman, KM
机构
[1] Univ Florida, Dept Neurol, Gainesville, FL 32611 USA
[2] Univ Florida, Dept Commun Sci & Disorders, Gainesville, FL 32611 USA
[3] Univ Florida, Dept Neurosurg, Gainesville, FL 32611 USA
[4] Univ Florida, Dept Clin & Hlth Psychol, Gainesville, FL 32611 USA
[5] Univ Kentucky, Dept Neurol, Lexington, KY 40506 USA
关键词
conduction aphasia; cortical stimulation; arcuate fasciculus;
D O I
10.1006/brln.1999.2135
中图分类号
R36 [病理学]; R76 [耳鼻咽喉科学];
学科分类号
100104 ; 100213 ;
摘要
Wernicke, and later Geschwind, posited that the critical lesion in conduction aphasia is in the dominant hemisphere's arcuate fasciculus. This white matter pathway was thought to connect the anterior language production areas with the posterior language areas that contain auditory memories of words (a phonological lexicon). Alternatively, conduction aphasia might be induced by cortical dysfunction, which impairs the phonological output lexicon. We observed an epileptic patient who, during cortical stimulation of her posterior superior temporal gyrus, demonstrated frequent phonemic paraphasias, decreased repetition of words, and yet had intact semantic knowledge, a pattern consistent with conduction aphasia. These findings suggest that cortical dysfunction alone may induce conduction aphasia. (C) 1999 Academic Press.
引用
收藏
页码:1 / 12
页数:12
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