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Dyslexia May Be Caused by Signal Processing Problem in Brain
Researchers hope study findings will lead to more treatment options
FRIDAY, Aug. 10 (HealthDay News) -- The learning disability dyslexia is caused by a problem with signal processing involving speech recognition in the brain, according to a new study.
Although they do not lack intelligence, people with dyslexia have trouble reading, understanding and explaining individual words or entire texts. Researchers in Germany found this is because a part of their brain's thalamus -- called the "medial geniculate body" -- does not process speech sounds correctly.
"This malfunction at a low level of language processing could percolate through the entire system. This explains why the symptoms of dyslexia are so varied," Begona Diaz, from the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig, said in an institute news release.
The researchers conducted two experiments. First, participants were asked to perform speech-comprehension tasks. Using magnetic resonance tomography, the researchers found abnormal brain responses during tasks that required the recognition of speech sounds.
In contrast, when the participants only had to listen to speech sounds and not perform a certain task, the researchers found no differences between the people who had dyslexia and those who didn't.
"The problem, therefore, has nothing to do with sensory processing itself, but with the processing involved in speech recognition," Diaz explained. "Recognizing the cause of a problem is always the first step on the way to a successful treatment."
Although there is no cure for dyslexia, it can be treated, the researchers noted. They concluded their findings could lead to improved treatment options for people with the condition.
The study was published online Aug. 6 in the Proceedings of the National Academy of Sciences.
Visit the U.S. National Institutes of Health for more on dyslexia.
Source: SOURCE: Max Planck Institute for Human Cognitive and Brain Sciences, news release, Aug. 6, 2012
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