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There is a PowerPoint file available to accompany this presentation. The BDA Conference 2001 CD-ROM contains 61 PowerPoint files. For details of how to obtain the CD-ROM, please contact the BDA.
Saturday stream K Session 09.00 - 09.45 Length 25 minutes
Al Galaburda
Beth Israel Hospital, Boston, USA agalabur@caregroup.harvard.edu
Abstract
Developmental dyslexia is characterized in most patients with the disorder by a difficulty performing tasks of phonemic awareness. Some experts believe that this difficulty arises initially from a problem with general sound processing, particularly fast changing sounds. Others claim that the problem is the result of a specifically linguistic anomaly, and that general sound processing problems are irrelevant. Both autopsy studies of dyslexia and brain activation studies in living subjects implicate dysfunction in large areas of brain, some of which are concerned with language, others with general sound processing. Animal models indicate that induction of cortical malformations such as those seen in dyslexic brains can lead to sound processing anomalies and anatomic changes in the thalamus. There is brain plasticity involving the auditory thalamus in animals that have incurred cerebral cortical malformations at birth. Males with this condition exhibit deficits in rapid sound processing, which can be demonstrated behaviorally in learning paradigms and startle reduction paradigms, as well as physiologically using evoked auditory potentials. Affected animals are impaired in processing rapidly changing sounds when lesions similar to those seen in dyslexic humans are produced in the cerebral cortex. They also show cognitive deficits from the same cortical lesions. The sex difference is interesting and is modulated by male sex hormones. This collection of findings will be reviewed and illustrated during the talk and implications for the understanding of developmental phonological dyslexia in humans will be discussed.
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