Brain Differences Linked to Dyslexia

Genetic Abnormalities May Contribute to Reading Difficulties

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Aug. 24, 2004 -- People with an inherited form of dyslexia may have less of the gray matter in the brain that's needed to process language, a new study suggests.

Researchers say the findings lend support to the notion that genetic abnormalities in the brain may contribute to the reading difficulties associated with dyslexia. Although the cause of dyslexia is unknown, the condition tends to run in families.

The study used new brain imaging techniques to show that people with dyslexia who also had a close relative with the learning disability had less gray matter volume in areas of the brain associated with language processing compared with people without reading problems.

Gray matter is the part of the brain that processes thinking skills and contains brain cells. White matter in the brain consists of nerve cells that link different areas of the brain and spinal cord and allow them to communicate with each other.

Dyslexia Tied to Brain Differences

In the study, published in the Aug. 24 issue of Neurology, researchers used an advanced testing method called voxel-based morphometry (VBM) to measure the volume of gray and white tissue in the brains of 10 people with inherited dyslexia and 11 healthy individuals without dyslexia.

Researchers say VBM is more precise than other imaging methods because it looks at the whole brain and detects volume and density differences.

The testing revealed significant gray matter abnormalities in many parts of the brain necessary for reading development among the people with dyslexia.

Researchers say previous studies that used MRI scans have suggested that intensive remedial reading therapy may help increase activity in these areas of the brain needed to process language. They say these results add further support to this view, and they recommend intensive reading therapy to correct the reading problems associated with dyslexia.

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SOURCES: Brambati, S. Neurology, Aug. 24, 2004; vol 63: 742-745. News release, American Academy of Neurology.
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