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Abstract:
Dual-route models of speech production suggest that
high-frequency forms are encoded in different ways from
low-frequency and novel forms. The frequent occurrence of some
words permits movement gestalts to be formed for the entire word.
More novel forms would be encoded through the on-line assembly
from sub-syllabic units - a process that is consistent with
generative symbolic-computational models. We propose that the
acquired neurological disorder of apraxia of speech (AOS)
provides a window to speech encoding mechanisms and that the
disorder represents an impairment of whole word storage
mechanisms. Previous studies with control and AOS speakers have
suggested that whilst high- and low-frequency words have
different durational characteristics in control speakers,
speakers with AOS showed no systematic effect of frequency on
speech output.
In this paper, we report the results of an investigation into
the durational characteristics of high- and low-frequency words
with a further control group of speakers with dysarthria. This
study revealed that the speakers with dysarthria performed in a
similar manner to normative control and left-hemisphere lesioned
aphasic but non-apraxic controls. These results suggest that the
abolition of frequency effects in the output of AOS speakers
found in previous studies was not due to a general motoric
impairment factor. This suggests that the disorder of AOS
provides an important test ground for models of speech
encoding.
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