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Atypical Brain Activity Detected in People with Dyslexia

Brain imaging studies at the National Institute of Mental Health (NIMH) have revealed dramatic evidence of a deficit in the brain's visual system in people with dyslexia, a disorder that affects the reading ability of millions of American school children and adults. While it has been commonly believed that only the language related areas of the brain are affected in dyslexia, this study adds to the growing body of research pointing to dysfunction of another portion of the brain known as V5/MT.

Using functional magnetic resonance imaging NIH scientists Guinevere Eden, D.Phil., and colleagues demonstrated in a small controlled study of adult males that people with dyslexia showed no activation in the V5/MT brain area, which specializes in movement perception. Dr. Eden's research confirms that people with dyslexia, hobbled by problems with reading, writing, and spelling, have trouble processing specific visual information. "We found that maps of brain activity measured while subjects were given a visual task of looking at moving dots were very different in individuals with dyslexia compared to normal control subjects," said Dr. Eden.

The eight control subjects showed robust activity in brain region V5/MT when viewing a moving dot pattern. Almost no activity was present in those areas in people with dyslexia. In fact, a clear finding in all six subjects showing no response in the V5/MT area is a step toward improving the understanding, diagnosis, and eventually, treatment for the disorder.

"This research confirms that dyslexia is a discrete brain disorder, not, as some people have believed, a by-product of a poor education," said NIMH Director Steven H. Hyman, M.D. Furthermore, if confirmed by additional research, functional brain imaging may be used as a tool for early and accurate diagnosis of this common and disabling disorder.

Whether the motion perception deficit uncovered by this study contributes to the reading disability characteristic of dyslexia is still unknown. "It is possible that the visual disturbances we found and the reading disturbances others have found may be caused by an underlying, common information processing deficit," said Dr. Eden. According to the research team, the anatomical changes underlying these functional differences are thought to occur during the early stages of development, when regional functional specialization occurs. Abnormal function in the specialized brain area V5/MT explains previously reported visual behavioral problems in dyslexia.

Future research will provide further insights into the details of visual and language deficits and their effects on reading. Dr. Eden's study suggests a broader definition of the underlying mechanisms of dyslexia, thus opening the way for development of special help and effective treatment for more people with the disorder.

All of the dyslexic subjects in this study had a childhood history of reading disability, a measurable reading deficit, a discrepancy of at least 2 standard deviations between their reading and verbal IQ, and poorer phonological awareness compared to controls, and none had neurological disorders. Normal controls were closely matched to dyslexics in age, education, socio-economic status, and IQ.

The technique of functional magnetic resonance imaging is based on the principle that blood flow, rich in oxygen, increases locally in active areas of the brain. Usually used to obtain information on structural details of the brain, fMRI can also pinpoint regions where oxygenation levels are changing as a result of neural activity. The procedure is noninvasive, as it exploits a magnetic tracer, namely hemoglobin, that is a normal constituent of blood.

The study, "Abnormal Processing of Visual Motion Processing in Dyslexia Revealed by Functional Brain Imaging," was published July 4 in Nature. Coauthors are Judith M. Rumsey, Ph.D., and Jose Ma. Masog, M.D., of NIMH, Thomas A. Zeffiro, M.D., Ph.D., and John W. VanMeter, Ph.D., of Sensor Systems, Inc., and Roger Woods, M.D., of U.C. L.A.

Information provided by the NIMH.
July 1996