Wernicke, and later Geschwind, posited that the critical lesion in conducti
on aphasia is in the dominant hemisphere's arcuate fasciculus. This white m
atter 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 induce
d by cortical dysfunction, which impairs the phonological output lexicon. W
e observed an epileptic patient who, during cortical stimulation of her pos
terior superior temporal gyrus, demonstrated frequent phonemic paraphasias,
decreased repetition of words, and yet had intact semantic knowledge, a pa
ttern consistent with conduction aphasia. These findings suggest that corti
cal dysfunction alone may induce conduction aphasia. (C) 1999 Academic Pres
s.