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Georgetown Researchers To Present Evidence Of Biological Cause Of Dyslexia

Date:
February 16, 2001
Source:
Georgetown University Medical Center
Summary:
Addressing a long-standing controversy concerning the causes of reading disability, a series of research studies done by a team at the Georgetown Center for the Study of Learning indicate that the areas of the brain used for reading are the same areas used for other visual tasks, and that these areas may not work properly in the brains of people with dyslexia.

Washington, DC -- Addressing a long-standing controversy concerning the causes of reading disability, a series of research studies done by a team at the Georgetown Center for the Study of Learning indicate that the areas of the brain used for reading are the same areas used for other visual tasks, and that these areas may not work properly in the brains of people with dyslexia. However, the researchers also found that an intensive, phonologically based reading intervention program could not only improve reading skills in dyslexics, but could also effect changes in brain activity that can be measured using functional magnetic resonance imaging (fMRI) technology.

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"These study results are further evidence that dyslexia has biological roots," said Guinevere Eden, DPhil, co-director of the Georgetown Center for the Study of Learning. "The results are significant because they could one day lead to the creation of an early diagnostic test for dyslexia that might allow us to identify the condition in children even before reading difficulties are present, and thereby intervene early to treat the disorder."

In their first study, Eden and Thomas Zeffiro, M.D., Ph.D., also a co-director of the Center, used fMRI technology to scan the brains of 37 participants-20 with dyslexia and 17 without the disorder-and found that each participant used similar brain areas for reading as he or she did for processing visual motion (identifying the direction of moving dots on a screen). They also found, however, that the dyslexic group activated these brain areas less strongly than the control group did while performing both these two tasks (reading and visual motion detection).

It appears that dyslexic participants-who, by definition, have difficulties reading-also experience difficulties in processing visual motion, and that the areas of the brain used by non-dyslexics to perform these two tasks may be damaged or not working in dyslexics.

"Unfortunately, today we are able to diagnose dyslexia only after children have shown difficulty in learning to read, usually around the time they're in second or third grade," said Thomas Zeffiro, M.D., Ph.D., also co-director of the Center. "But, if we know that the same areas of the brain used for reading are also used to perform other types of visual tasks, then we can test children before they reach reading age to determine whether those areas work properly. A biological marker of this type might give us the chance to intervene before reading failure has occurred." Zeffiro and Eden both stressed that identification of a presymptomatic biological marker for dyslexia is not that far along yet, and that any diagnostic test that might be developed would not be available until further, larger-scale studies had been completed.

In another study, Eden and Zeffiro-working with Frank Wood, Ph.D., and Lynn Flowers, Ph.D., of Wake Forest University Medical Center at Bowman Gray in North Carolina-found that a reading intervention program could produce measurable improvements in reading skills and related changes in neural activity that are observable using fMRI.

In this study, Eden, Zeffiro and their colleagues studied 20 adults with a lifelong history of dyslexia. They divided the adults into two groups of 10 and conducted baseline brain scans on both groups. One group then participated in an intensive eight-week interventional program designed to improve reading skills, while the other group received no intervention at all. At the end of the eight-week period, brain scans showed that the group that had taken part in the reading program showed measurable improvements in reading and related changes in neural activity. The brain scans of the control group showed no differences.

"It was quite exciting to be able to see such clear confirmation of our hypothesis in the fMRI scans," Eden said. "This is a great step towards better understanding the neural mechanisms involved in reading and learning."

Zeffiro and Eden and their colleagues from the University of Pittsburgh, Wake Forest University School of Medicine-Bowman Gray, and Harvard Medical School, will present these findings at the annual meeting of the American Association for the Advancement of Science (AAAS) on February 16 in San Francisco, Calif.

Georgetown University Medical Center is one of the nation's preeminent institutions of medical research and education. It includes a biomedical research enterprise as well as the nationally ranked School of Medicine, and the School of Nursing and Health Studies. The federally funded Georgetown Center for the Study of Learning seeks to better understand the neural mechanisms that enable the acquisition of reading skills, and to identify new approaches to assess and treat reading disabilities.


Story Source:

The above story is based on materials provided by Georgetown University Medical Center. Note: Materials may be edited for content and length.


Cite This Page:

Georgetown University Medical Center. "Georgetown Researchers To Present Evidence Of Biological Cause Of Dyslexia." ScienceDaily. ScienceDaily, 16 February 2001. <www.sciencedaily.com/releases/2001/02/010216081104.htm>.
Georgetown University Medical Center. (2001, February 16). Georgetown Researchers To Present Evidence Of Biological Cause Of Dyslexia. ScienceDaily. Retrieved November 27, 2014 from www.sciencedaily.com/releases/2001/02/010216081104.htm
Georgetown University Medical Center. "Georgetown Researchers To Present Evidence Of Biological Cause Of Dyslexia." ScienceDaily. www.sciencedaily.com/releases/2001/02/010216081104.htm (accessed November 27, 2014).

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