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2009 | 45 | 2 | 313-326

Article title

A Biological basis for Aphasia Treatment: Mirror Neurons and Observation-Execution Matching

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Abstracts

EN
Aphasia is caused by damage to the human brain, and recovery requires adaptive changes to the structure and function of this organ. Despite this obvious fact, biology plays little role in rehabilitation of persons with aphasia. Although linguistics can be useful in characterizing aphasic behaviour, thus providing a way to assess the effects of therapy, there is little evidence to suggest that linguistic models of impairment can themselves form the basis of effective therapy.Biological evidence from primates has demonstrated the presence of neurons that have both visual and motor properties, which discharge both when an action is performed and during observation of the same action. We postulate that behavioural stimulation of this system may play an important role in motor learning for speech and thereby aid language recovery after stroke.IMITATE is a computer-assisted system for aphasia therapy based on action observation and imitation. IMITATE therapy consists of silent observation of audio-visually presented words and phrases spoken aloud by six different speakers, followed by a period during which the participant orally repeats the stimuli. The treatment approach is motivated by the physiology of the brain in an effort to change specific anatomical connections, and the treatment method draws strongly from psychological evidence on learning.IMITATE is currently being used in a clinical trial, and results will not be known until these data are available in late 2010. At that juncture, it will be possible to evaluate fully the efficacy of IMITATE and to inform theoretically about the mechanism of action and the role of a human mirror system in aphasia treatment.

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Year

Volume

45

Issue

2

Pages

313-326

Physical description

Dates

published
2009-06-01
online
2009-06-25

Contributors

author
  • The University of Chicago

References

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Publication order reference

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bwmeta1.element.doi-10_2478_v10010-009-0017-3
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