Apraxia of speech (AOS) and conduction aphasia are commonly caused by left hemisphere stroke and often severely affect speech production. Although the clinical profile involved in these disorders is different, the most effective methods for managing them are unclear and many patients with AOS or conduction aphasia show limited recovery despite intensive treatment. We suggest that the underlying impairment in both AOS and conduction aphasia is poorly understood and propose a new framework for characterizing both disorders. Building on our previous research as well as the latest models of speech perception and production, this project will examine the neural bases of AOS and conduction aphasia. The result should be increased understanding of normal and disordered speech/language processing as well as offer new insights into rehabilitation of these two poorly understood disorders. Although the critical lesion locations associated with AOS and conduction aphasia have been controversial, recent studies suggest that damage to Broca's area and the left posterior inferior parietal lobe cause AOS and conduction aphasia, respectively. Along with others, our research has identified Broca's area as playing a role in not only the production of speech but also in the visual perception of others'speech motor movements. Similarly, recent studies (including our own) suggest that the left posterior inferior parietal lobe plays a critical role in speech processing as an interface between auditory speech and motor speech output. These findings suggest that individuals with AOS and conduction aphasia have an impaired speech perception component that may negatively affect recovery efforts aimed at improving speech production. Although this previous research has important theoretical and practical implications for understanding the neural basis of human communication as well as the nature of AOS and conduction aphasia, further study of this issue is imperative. This project will involve testing of a large group of stroke patients with left hemisphere damage as well as transcranial magnetic stimulation (TMS) to examine the effect of permanent (brain damage in stroke patients) and transient (TMS in normal participants) cortical interruption on speech processing. The long-term goals of this research are to better understand the neural bases of AOS and conduction aphasia. Treatments aimed at improving speech production in patients with AOS or conduction aphasia have traditionally proceeded with the assumption that speech perception is intact in both disorders. Therefore, it is crucial to understand the relationship between impaired speech production and perception in AOS and conduction aphasia. As a result, future treatments of thes frustrating and recovery resistant disorders can be greatly improved.

Public Health Relevance

Apraxia of speech (AOS) and conduction aphasia are stroke related speech impairments which are extremely resistant to behavioral therapy, even when intensive treatment is applied. The purpose of this research is to study the underlying brain damage and impairment associated with AOS and conduction aphasia. As a result of this research, we will be able to study how stroke patients with AOS or conduction aphasia can be better rehabilitated to maximize their potential for recovery.

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Research Project (R01)
Project #
5R01DC009571-04
Application #
8213598
Study Section
Language and Communication Study Section (LCOM)
Program Officer
Shekim, Lana O
Project Start
2009-02-25
Project End
2013-01-31
Budget Start
2012-02-01
Budget End
2013-01-31
Support Year
4
Fiscal Year
2012
Total Cost
$294,210
Indirect Cost
$77,480
Name
University of South Carolina at Columbia
Department
Other Health Professions
Type
Schools of Public Health
DUNS #
041387846
City
Columbia
State
SC
Country
United States
Zip Code
29208
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Fedorenko, Evelina; Fillmore, Paul; Smith, Kimberly et al. (2015) The superior precentral gyrus of the insula does not appear to be functionally specialized for articulation. J Neurophysiol 113:2376-82

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