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DYSLEXIA FROM SCRATCH
The Jigsaw
Puzzle
The history of how schools deal with dyslexia has been
a very boring story because for forty or more years, there
was nothing to say. Dyslexia was actually identified by Samuel
Orton as a separate phenomenon way back in 1925, but even
today, eighty years later, almost nobody in the educational
field has a clue as to what causes it, never mind what to
do about it. Sam did his bit by realizing that there were
bright people with an oddball reading problem that had nothing
to do with intelligence, and he was right in that. But he
was wrong in thinking that when someone with “strephosymbolia,” as
he called it, misread was for saw it was because the right
hemisphere was doing “mirror reading” or reversing
the letters. He was wrong about that, but it stuck, and to
this day, people will tell you that dyslectics reverse letters
when they read. (More of that later.)
But he did something else that turned out to be very important.
He insisted that treatment required a good dose of phonics.
This was in a time when the country had gone berserk over
that educational disaster called “Whole Language” which
effectively produced several generations of normal kids who
were, nevertheless, poor readers. Phonics was a dirty word
in “Whole Language” teaching, but Sam realized
that a dyslectic reader had to have it, so he and his friend,
Anna Gillingham, devised an excellent phonics program that
is still used in special education classes today and has
spawned a world-wide institute called the International Dyslexia
Association.
In the meantime, with the predictable swing of the pendulum
that characterizes educational theories, Whole Language disappeared,
phonics came back in fashion, and miraculously American children
began to learn to read again. But the dyslectic ones didn’t.
Suddenly they stuck out of the crowd, and it became clear
that phonics, although vital, was not enough, because there were all those
dyslectic kids-- still there -- and still not reading.
Fast forward through 50 years of nothing to say, to the
post-war boom in technological innovation, but don’t
look for the new research in neurology to be directed at
the plight of the hapless dyslectics. Hints about what might
account for the reading problem came dribbling in in dribs
and drabs of disconnected pieces of information, from every
field you can think of except reading research. Like pieces
of a jigsaw puzzle, one piece of information would turn out
to fit another little piece. But virtually nobody gathered
it all up and morphed it into effective teaching techniques.
For instance, isolated bits of technical information drifted
in from:
• research on epilepsy
• timing of interhemispheric transfer across the corpus callosum
• research by a psychiatrist using high speed photography on athletes (!)
• anomalous double regressions in dyslectic eye motions
• research on magno and parvo cells in the visual and auditory systems
• realization of the plasticity of the brain
• efforts to develop 3-D television
• meditation studies on Buddhists monks
• depression
• ADD and ADHD
• studies on stroke victims
The trouble was that scientists in one field didn’t connect bits of their
information to the results from other fields so they didn’t see
a pattern that had anything to do with correcting dyslexia.
The first real breakthrough came from work on epilepsy,
done by Michael Gazzaniga and Roger Sperry in the 60’s,
in which they sectioned the central bridge of tissue in the
brain called the corpus callosum that connects the two hemispheres.
Cutting the communication between sides was done to prevent the transfer
of an electrical storm in one hemisphere to the opposite
hemisphere, where it would cause a seizure. The surgery not
only controlled the epilepsy, it produced people whose left
and right halves of the brain were out of communication with
each other. With the two isolated, the doctors could find out what
each side could do without interference from the other.
When this information was published in Scientific American,
I was teaching six dyslectic junior high school boys.The
linguistic specialties of the left hemisphere turned out
to be phonics, phonemic awareness, syntax, grammar, and letter
sequencing. These were exactly the things my boys couldn’t do,
so I sensibly concluded that they weren’t using their left hemispheres.
It also cleared up the mistaken notion that dyslectics see things backwards.
What is going on is that their reading was being done largely by the right
hemisphere, which is cheerfully unconcerned whether the letter order it sees
matches the sounds it makes. One of my students, when I dictated DOWN, wrote
OWDN and looked at me, puzzled, as if to say, “You got a problem with
that?” His right side saw the shapes of the letters, concluded they were
all there and didn’t care that the sound order didn’t match the
letter order. In fact, it didn’t even know what sounds went
with which shapes.
Serendipitously, a researcher named Doreen Kimura happened
to be experimenting with a dichotic procedure using stereo
earphones to send different auditory signals simultaneously
to the two hemispheres. So I began hopefully sending music
to the boys’ right hemispheres and a phonics exercise
to the left simultaneously to see whether I could isolate
and train that unused language area. The results at the end
of the year were so astonishing that my supervisor accused
me of fudging the scores! Fortunately for me, not everybody
was so suspicious. Still, I suspect that The Journal of Learning
Disabilities did startle a lot of people when they published
an account of the program in 1977.
The beauty of Kimura’s dichotic procedure was twofold.
It enabled me to both train the left hemisphere and at the
same time, by-pass the CC. With the dichotic procedure, each
ear sent a signal directly to the opposite hemisphere and
there it stayed. So I reasoned that if the kids could not
read when they were using the CC and could read if it were
by-passed, it looked very much like a big part of the problem.
A couple of years later another piece of the puzzle turned
up that again implicated the CC. A psychiatrist in Boston
had been experimenting with high-speed photography of athletes.
As a side line, he began taking high-speed movies of dyslectic
and autistic children and discovered one of the most important
clues to the problem of dyslexia up to that time. It seems
that dyslectic children are out of sync with themselves right
down the midline of the body. When they blink, one eyelid
starts down a couple of milliseconds before the other. When
they smile, one corner of the mouth starts up the same number
of milliseconds before the other. When they turn toward a
click, one side begins to turn the same number of milliseconds
before the other. It all happens so fast that it takes high-speed
photography to catch it. But apparently the brain is getting
the primary signal and then a couple of milliseconds later,
a secondary, weaker one comes across that slow corpus callosum.
Because the delay is the same for each modality—visual, auditory, or kinesthetic,-- one conclusion that
can be drawn is that the secondary signal coming across the CC is late. The
psychiatrist’s theory was confirmed much later when some
of the first brain scans indicated that the CC was, indeed, a
slow transmitter of information.
Certain double regressions in
the eye movements of dyslectics that the psychiatrist-photographer
also found became confirmed later wth a device called an Ober
Visagraph, which both recorded and graphed these double regressions.
Instead of making smooth saccadic motions while the student
is reading, the dyslectic’s eyes flick
back twice to the previous word(s) before going on. The difference between
smooth normal reading and the back and forth motions of the dyslectic’s
eyes is so dramatic that it is almost a definitive diagnosis
of the problem. Again a weaker, late signal is the culprit.
One of the top British specialists in visual dyslexia found
another possible source of slow information transfer. In
the visual system there are two kinds of cells, parvo and
magno. The larger the cell, the faster it works, and the
magnos are faster than the parvos. But in dyslexia, the magnos
are not as large as they should be, implying that they will
transmit more slowly than they should.
So here’s how things stood. Slow interhemispheric
transfer of visual and auditory information was sending out-of-sinc
input to a specific language area in the left hemisphere
called the angular gyrus. This was partly due to a badly
shaped and/or slow corpus callosum. By-passing the faulty
CC, and instead sending one, clear auditory signal to the
angular gyrus improved reading so dramatically that in one
or two years of training, kids could be brought up to grade-level
reading. This was the first breakthrough since Sam Orton
insisted on teaching phonics to dyslectics. And it explained
why even the best phonics was not enough. The phonics lesson
had to be delivered to the correct area of the brain for
processing. And it needed to be delivered up to speed, which
meant by-passing the CC.
Now fast forward again to the last ten or fifteen years,
when two things happened. One was the invention of a brain
scan called an fMRI. Plain old MRI’s
had been around for awhile, but they merely took a picture. The fMRI was more
like a movie camera. It could take pictures of what was going on in the brain
while a person was thinking. FMRI’s have become the most exciting tool
available to neurologists in years, and they are using them to investigate
everything they can think of -- even dyslexia! FMRI’s
from around the world have now shown conclusively that that
left angular gyrus is not used when a dyslectic person reads,
whereas it lights up like a Christmas tree when a normal
one does. Finally at least one big piece of the puzzle is
firmly in place.
Now two questions remained. Can you increase use of the
left angular gyrus, and if so, how do you do it? The answer
to the first question is yes, it is possible to increase
activity in one hemisphere in isolation from the other, just
as Dora Kimura did fifty years before. This has been accomplished
during research on both strokes and on depression. The neurologist’s techniques
are to numb one hemisphere with magnetic pulses while they test or train the
other. Numbing half of a student’s brain (even unintentionally)
is not an approved technique for public school teachers,
but we can mechanically accompish much the same thing by
sending the right hemisphere some nice Mozart to listen to
while the other side gets its phonics lesson. For the first
time, these studies proved conclusively that you can give
private lessons to one hemisphere, and our success in teaching
reading hinted that we were doing just that.
So far, so good.
But reading involves vision as well as hearing, and although
the architecture of the brain allows us to isolate an auditory
signal to one hemisphere, isolating visual input to only
one hemisphere during reading is tricky. Reading requires
using the fovea of the retina, and the fovea sends its input
to both hemispheres at the same time, and that’s that.
For over thirty years I have wished in vain that I could
find a way to stimulate the left language areas with a visual
signal as well as an auditory one. Recently some intriguing
information from people trying to produce 3D TV without colored
glasses has indicated that I may have been going at it backwards.
Instead of actually cutting out the slow one and using only
the fast signal, it now appears that instead, you can simply
speed up the slow one! How? Just by making it brighter. It
seems that a brighter visual signal travels faster than a
darker one.
Again, a dib of information from one field has
fitted neatly with a dab from another. The question for me
was how to apply it. Fortunately I wasn’t
the only one who wanted to increase activity in the left
hemisphere using visual input. Stimulation of the left hemisphere
appears to have a profound effect on reducing depression
and ADD. So two psychiatrists dealing with seriously depressed
patients have been using some glasses that actually enable
a brighter signal to go to the left hemisphere than to the
right.
There is yet another way of activitating the left side
which also produces a cheerful calmnesss which is useful
in reducing both depression and ADD. It is the kind of meditation
practiced by Buddhist monks, and it suffuses the left side
with gamma waves which do the calming. But learning to meditate
effectively can take years. Again, not practical for school
teachers. On the other hand, virtually all dyslectic people
are somewhat depressed, usually from being considered damaged
goods by their contemporaries. And millions of kids are annually
misdiagnosed with ADD or ADHD just because they can be twitchy
and forgetful. Because hyperactivity and depression are such
frequent concomitants of dyslexia, the calming and cheering
effects are invaluable extras for dyslectic students.
So today we have two sources of slow transmission that
upset the finely coordinated timing between the two hemispheres
needed for skillful reading: a misshapened corpus callosum
and undersized magno cells in the visual system. Which contributes
more to the problem? No one knows. But it is now possible
to end run them both and teach a dyslectic student to read
in somewhere between four or five months to a year or so.
When he comes in for his lesson, you put him in the special
glasses for his phonics lesson and you put him in the stereo
earphone set up for his spelling lesson. You use a carefully designed program like Reading
from Scratch that focuses heavily on the five big problems--
phonics, phonemic awareness, syntax, grammar, and letter
order-- and before you know it, he is reading. And happy.
So are the tax-payers.
It is ironic that it took eighty years to close the gap
between educators and the scientists who have solved the
problem. Talk about slow transmission! Eighty years for a
two millisecond difference.
One question is still unanswered, leaving us with a small
part of our jigsaw puzzle unsolved. We know how to treat
dyslexia now, but we still don’t
know how to prevent it in the first place. The answer to that will probably
come from genetic research in the future. Its makes sense that some gene controls
the development of the corpus callosum and the size of the magno cells. But
manipulating genes is far into the future. When that finally happens, dyslexia
can be considered cured and relegated to the history books as something that
once was a “handicap.”
Dorothy van den Honert
115 Mountain Drive, Pittsfield, Mass. 01201
tel: 413-442-2687
e-mail: info@dyslexia.org
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