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Abstract:
We have proposed a new model of the functional anatomy of
language (Hickok & Poeppel, 2000, TICS, 4:131-8) which includes
as two of its components (i) a system in the posterior STG
bilaterally which constructs a sound-based representation of
speech, and (ii) a more strongly left lateralized system in cortex
in the temporal-parietal-occipital junction which serves to
interface sound-based representations in pSTG with widely
distributed conceptual-semantic representations. The model holds
that the left pSTG also participates in phonemic aspects of speech
production. Here we show how damage to different components of this
model can account for the symptom clusters of the fluent aphasias.
Total destruction of the system supporting the construction of
sound-based representations of speech (bilateral pSTG lesions) will
produce profound deficits in speech perception (word deafness).
Left lesions involving the pSTG will yield a syndrome with good
auditory comprehension, because right pSTG is still functioning,
but with phonemic errors in production (conduction aphasia). Left
T-P-O lesions will produce auditory comprehension deficits and
semantic errors in production, because of a breakdown in the
mapping between sound and meaning, but with preserved phonemic
production processes (transcortical sensory aphasia). Lesions to
both left pSTG and T-P-O will yield a combination of symptoms found
in conduction and transcortical sensory aphasias, with poor
auditory comprehension, and a mix of phonemic and semantic errors
in production (Wernicke's aphasia).
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