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Dyslexic Children's Brains Differ From Normal Kids'
Dyslexia, a reading disorder, is the most common learning disability,
affecting an estimated 5 percent to 15 percent of children. Now a new
interdisciplinary study shows that dyslexic children use nearly five times
the brain area as normal children to perform a simple language task.
The study also shows, for the first time, that there are chemical
differences in the brain function of dyslexic and non-dyslexic children.
The research, published in the current issue of the American Journal of
Neuroradiology by an interdisciplinary team of researchers at the University
of Washington, also provides new evidence that dyslexia is indeed a
brain-based disorder.
The researchers, headed by developmental neuropsychologist Virginia
Berninger and neurophysicist Todd Richards, used a novel noninvasive
technique called proton echo-planar spectroscopic imaging (PEPSI) to explore
the metabolic brain activity of six dyslexic and seven non-dyslexic boys
during oral language tasks.
PEPSI is about 32 times faster than conventional magnetic resonance
spectroscopy. Software developed at the university enabled the researchers
to detect specific brain chemicals, including lactate.
Lactate is a by-product of energy metabolism produced by neurons when the
brain is activated. The study measured levels of brain lactate activation.
Most, but not all, of this brain activity took place in the left anterior,
or frontal, lobe of the brain, which is known to be one of the centers for
expressive language function.
"The dyslexics were using 4.6 times as much area of the brain to do the same
language task as the controls," said Richards, a professor of radiology.
"This means their brains were working a lot harder and using more energy
than the normal children."
"People often don't see how hard it is for dyslexic children to do a task
that others do so effortlessly," added Berninger, a professor of educational
psychology. "There are learning differences in children. We can't blame the
schools or hold teachers accountable for teaching dyslexic children unless
both teachers and the schools are given specialized training to deal with
these children."
The 13 boys in the study were between 8 and 13 years of age and the dyslexic
and control groups were well-matched in age, IQ and head size, but not in
reading skills. The controls were reading at a level above normal for their
age and had a history of learning to read easily. The dyslexics had delayed
reading skills and were reading well below average for their age. Their
families also had a history of multi-generational dyslexia that was
confirmed in a concurrent family genetics study.
Once fitted with earphones, the boys were asked to perform four tasks while
their brains were being imaged. Three of the tests involved pairs of words
and the fourth used pairs of musical tones.
In the language tests, the boys heard a series of word pairs that consisted
of pairs either of two non-rhyming words such as "fly" and "church," two
rhyming words such as "fly" and "eye," a non-rhyming real word and a
non-word such as "crow" and "treel," and a rhyming word and non-word such as
"meal" and "treel."
The boys were asked if the word pairs rhymed or didn't rhyme and if the
pairs contained two real words or one real and one non-word. They responded
by raising a hand to indicate yes or no. In the music test, the boys heard
pairs of notes and raised one hand if they thought the notes were identical
and the other if they believed them to be different.
While the dyslexic boys exhibited nearly five times more brain lactate
activation during a language task that asked them to interpret the sounds of
words, there was no difference in the two groups during the musical tone
test. This means the difference between the dyslexics and the normal
children relates to auditory language and not to nonlinguistic auditory
function, according to Richards and Berninger.
They also said the findings are important because they shed new light on
brain mechanisms involved with dyslexia at a developmental stage when it is
still amenable to treatment. In addition, the functional differences between
dyslexics and control subjects add evidence that dyslexia is a brain-based
disorder.
"When a child has a brain-based disorder it is treatable, although it may
not be curable, just as diabetes is," said Berninger. "Dyslexia is a
lifelong condition, but dyslexics may learn to compensate for it later in
life. We know dyslexia is a genetic and neurological disorder. It is not
brain damage. "Dyslexics often have enormous talents in other parts of their
brain and shine in many fields. Einstein was a dyslexic, and so were
inventor Thomas Edison and financier Charles Schwab.
"While it is useful to show there are brain differences between dyslexic and
non-dyslexic children, considerably more research is needed to precisely
define the chemical and neurological markers of dyslexia. What we found is a
metabolic marker, but there could be a more fundamental cause. We need to
understand the molecular and neural mechanisms underlying dyslexia," she
added.
Other members of the UW research team and co-authors of the study are
Stephen Dager, professor of psychiatry and behavioral science; David Corina,
assistant professor of psychology; Cecil Hayes, professor of radiology;
Robert Abbott, professor of educational psychology; Susanne Craft, adjunct
associate professor of psychiatry and behavior science; Dennis Shaw,
assistant professor of radiology; and Stefan Posse, affiliate assistant
professor of radiology. In addition, UW doctoral students Sandra Serafini,
Aaron Heide, Keith Steury and Wayne Strauss participated in the research.
The study, part of a wider UW effort to understand the basis of dyslexia and
develop treatments for it, was funded by the National Institute of Child
Health and Human Development (NICHHD).
[Contact: Virginia Berninger, Todd Richards]
04-Oct-1999
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