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Deficit In Brain Activity Is Linked To Dyslexia

By Steve Connor, The Independent, London

LONDON -- A region of the brain known as the body's autopilot, because it allows us to carry out complex movements without thinking too hard, has been linked to dyslexia, the learning disorder that affects one child in twenty.

Scientists have identified abnormal activity in the cerebellum of dyslexics, which could account for why they must concentrate far harder on reading than non-dyslexic people, a finding that may lead to better pre-school tests for the condition.

The research could explain why dyslexic children tend to be more clumsy and why they find it more difficult to carry out ``automatic'' movements that other people take for granted, such as driving while talking, and playing sports such as tennis where movement in relation to other people or objects is important.

Rod Nicholson, a psychologist at the University of Sheffield who made the five-year study, told the British Association that several lines of evidence point to a ``deficit'' in the activity of the cerebellum as the probable cause of dyslexia.

``Of course automatization is a key requirement for reading, and there is extensive evidence that dyslexic children, even when reading well, are less fluent, requiring more time and effort to read than would a non-dyslexic child of the same reading age.

``We have used the analogy of driving in a foreign country - one can do it, but it requires continual effort and is stressful and tiring over long periods. On our account, life for a dyslexic child is like always living in a foreign country.''

The most startling finding, Professor Nicholson said, was that dyslexic children are significantly worse at balancing, a highly automatic ability not obviously connected to reading. ``We found that although a group of dyslexic adolescents were normally able to balance as well as non-dyslexic children their balance deteriorated very significantly when they had to do something else at the same time.''

Tests designed to reveal low cerebellum activity showed significantly greater ``deficits'' in 80 per cent of dyslexic children, a finding Professor Nicholson described as unexpected, because previous studies have concentrated on the cerebral cortex, which is known to be involved in learning.

A second study using a brain scanner revealed that dyslexic adults had 10 per cent of the cerebellum activity of non-dyslexics when performing tasks involving automatic control, namely learning a sequence of finger movements.

Professor Nicholson said an analysis of brains stored at the International Dyslexia Association Brain Bank in Boston, Massachusetts, found dyslexics had larger than average nerve cells in the cerebellum. ``We believe we now have a coherent account of the major symptoms, the underlying cause and the way the reading problems develop ... there appear to be remarkably few loose ends.

``If the underlying cause can be established, then it should be possible to diagnose dyslexia pre-school, thereby giving the opportunity to provide initial reading support better tuned to the way that dyslexia children learn best,'' Professor Nicholson said.


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