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Nerve Disorganization May Spur Form of Dyslexia

Brain scans show real differences, researchers say

TUESDAY, Dec. 4, 2007 (HealthDay News) -- Disorganized, meandering tracts of nerve fibers in the brain may cause a form of dyslexia marked by slow and choppy reading fluency, U.S. researchers report.

There are different forms of dyslexia, which affects 5 percent to 15 percent of children.

In this study, researchers at Children's Hospital Boston and Beth Israel Deaconess Medical Center used a special form of MRI called diffusion sensor imaging to study the brains of 10 people with dyslexia caused by a rare genetic disorder called periventricular nodular heterotopia (PNH), which disrupts brain structure. People with PNH have normal intelligence but have trouble reading smoothly because they lack the rapid brain processing needed for this aspect of reading.

They compared the PNH patients to 10 people with dyslexia without neurological problems and to 10 people without dyslexia who were normal readers.

As reported in the Dec. 4 issue of Neurology, the scans revealed a disorganized, wandering pattern of white matter nerve fiber connections in the brains of the PNH patients. The more disordered a patient's white matter nerve fiber connections, the less fluent or smooth their reading, the team noted.

"We looked at dyslexia caused by a particular genetic disorder, but what we found could have implications for understanding the causes of dyslexia in other populations as well," study co-leader Dr. Christopher Walsh, chief of the division of genetics at Children's Hospital Boston, said in a prepared statement.

Learning more about the link between brain structure and reading may help lead to the development of new techniques to improve reading skills in dyslexic children and adults with poor reading skills, the researchers said.

More information

The U.S. National Institute of Neurological Disorders and Stroke has more about dyslexia.

SOURCE: Children's Hospital Boston and Beth Israel Deaconess Medical Center, new release, Dec. 3, 2007
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