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Al Galaburda - What a great man! For years I have been singing his praises to my teenage dyslexic students:
"He was given some brains when their owners died, both dyslexic and non-dyslexic. Al cut them up and weighed them. Guess what, he found that although non-dyslexic brains had a larger left side and smaller right side, dyslexic brains had an equally large left side (as the non- dyslexic) but a slightly larger right side. So there you have it, dyslexics have more brains than non-dyslexics'." I then go on to say, "Al's work was cut short because he was very old and had died."
Therefore it was with considerable interest that I went to see my hero, hale, hearty, surprisingly youthful, standing on the stage talking to the conference on Saturday morning.
I can't say that I liked everything Al said, nor his attitude to small furry lab animals, but the science and implications of his speech are of outstanding importance.
His ideas and evidence will be a major driving force behind how dyslexics are assessed and remedied for years to come.
The big idea Al was trying to put over could be interpreted to be: There are faults in - not only the way dyslexics sort out incoming data (light into nerve impulses) before it gets to the brain; but also - how data is worked upon when it does get inside the brain (nerve messages into pictures in the mind's eye.
The two types of fault stem from the same initial cause. This could be damage to a piece of the surface of the thinking cap area of the brain before birth. The damage could be mediated through inherited dyslexia-susceptible genes.
No big idea is worth a hill of beans, if there is no evidence to back it up. Al's evidence was by use of an animal model. If the idea could be shown to be true for a rat, it is probable that it is also true in the human. There are strains of rats which have been found to be susceptible to dyslexia. That is, humans have wonky tissue in a certain piece of their visual cortex, and so do the rats.
The genetically susceptible baby rats had the membrane of that area of the brain surgically ruptured, very slightly. The rats to all intents and purposes grew up normally (until they met their demise).
However when their brains were examined, it was found that the original small wound had produced a limited batch of deviant small nerve cells akin to small batches of deviant nerve cells seen in dyslexic human brains. The deviant nerve cells had multiplied and spread like legs of a spider to distant parts of the brain. These neurones were parts of the working nerve pathways for distant and different functions. These thalamus based cells caused thalamus dysfunction's as the rats grew up. One thalamus function involves depression of brain chemicals, which damp down over-reaction in the brain (inhibitory neuro-transmitters).
Looking at the learning behaviours of the rats with the experimental lesions to the brain, there are clear parallels with the behaviours of language disordered humans.
The rats were trained so that they could poke their snouts into a food trough when they heard the second of two sounds, presented one after the other. When the sounds were given too close together, the rats could not distinguish the sounds as different. With a greater space between the sounds, they could tell the difference. This is the same temporal processing problem that dyslexic children have.
Now guess what? There was a gender difference - the males were worse at this task than the females were!
The rats were given a second task: on the second of the two sounds - the rats were to act startled.
Testosterone can be a neurotransmitter chemical. Many a male behaviour trait has been laid at the door of testosterone.
The genetically susceptible rats with brain lesions were divided up into three groups: males, females and females who had been given testosterone. Al found two things. Firstly that females without testosterone startled, but that males and females with testosterone took longer to startle. These rats showed a poor working memory.
The second finding was in the structure of the cells under the lesions. In the females without testosterone there were fewer, larger cells. In the males and females with testosterone, there were many smaller cells.
Testosterone is implicated in the development of the deviant cells. (Castration - I don't think so. Female hormones are modified from testosterone.)
The model suggests genetic difference leads to damage before birth, leading to later dysfunction in areas distant to the Thalamus. There are greater numbers of males affected than females.
The evidence from what can be seen - anatomy abnormalities, is causally related to poor working memory, behavioural abnormalities at multiple levels, hormonally modulated difference between males and females.
Great ideas, great science. What didn't I like about it? I wanted Al to tell us something about why it's great to be dyslexic, how dyslexics have enhanced brain capacity. The reality of what he is saying is concerned with mal-formed genes, neural damage leading to learning and behaviour dysfunctions. We are bound to hear more of Al Galaburda's work in the future, not only as evidence of 'Dyslexia - the disability,' but also as the research is expanded to humans with investigations into neuro-protection, genetics, molecular studies and imaging studies.
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