A learning disability may be thought as a kind of ailment, difficulty, trouble, condition, even an illness in the eyes of some (with, sometimes, special gifts notwithstanding), and as such a special education teacher is a type of clinician.
Special education teacher as a clinician
We have a dictum in clinical medicine that states that we use treatments because they work, and not necessarily only because they make sense, and, as a corollary, we do not use them if they do not work, even though theory says they should work (change the theory!). Nonetheless, it is fun to have theories and it is useful to have them as a way, at least, to devise new treatments (hoping that they will work). And, clinicians are commonly interested in the causes of the illness or condition they work with. In the case of developmental dyslexia, and unlike the situation in the 80s and before, many scientists have become interested in dyslexia and its causes, and many theories have emerged, some of which may now be contributing to new ideas for treatments.
Theories and new ideas about dyslexia
Everyone intuits that reading comes through the eyes (unless you are reading Braille), and therefore the visual system could be implicated in dyslexia. As it turns out, based on more recent research, the visual system may indeed be dysfunctional, although it is not clear to what extent the visual problem contributes to the reading difficulty. Some recently published scientific papers show that manipulating the way visual information is provided during reading improves the success rate. Other articles show that playing some action games on your computer or handheld device improves reading ability. Still others have failed to demonstrate significant visual problems in dyslexia and have discarded this as a fundamental explanation. The truth must exist somewhere in the middle, and at least one explanation may be that not all dyslexics are the same. A convenient and ecumenical hypothesis would be that several systems contribute to learning to read and to reading (not entirely the same thing), and that mixes of deficits in all of these systems are needed for the clinical problem to emerge. In that case, helping out any one of the systems may be enough to get the problem somewhat taken care of.
A majority of researchers (whom the visual fans consider to be a mafia because they are powerful nowadays) are more inclined to blame the language system as the primary cause of dyslexia and pooh-pooh any visual explanation.
Phonetics and dyslexia
There are oodles of data showing some form of language problem in dyslexics, most of which having to do with phonology. Phonology is the study of the sound-structure of a language, and dyslexics have problem playing with language sounds (as in pig-latin and rhyming, for instance), which suggests that they do not know them well enough. However, phonology itself is a complex concept that contains sub-parts, which begs the question as to what part of phonology is involved. Some researchers, including this writer, believe that phonology can be subdivided into phonological grammar and phonetics, which are somewhat independent from each other in principle and in the brain systems that support them. The phonological grammar is the part of phonology that has to do with what sounds go together legally in a particular language (for instance, in English no word has the structure “lc” at the start, but “cl” is allowed, e.g., click, clack, clock). It appears that dyslexics are capable of learning these types of grammatical rules.
On the other hand, they are bad at speech perception, and, in one study, they even showed difficulty distinguishing a natural language from a machine-generated one. As this part of phonology, phonetics, implicates perception, rather than only the cognitive aspects of language, it is reasonable to suggest that dyslexia may originate from the dysfunction of very low level acoustic processors in the brain, soon after a sound first impinges on it at the brainstem, just in from the inner ear.
What does study of the brain have to say about these questions and debates?
Well, the study of the brain is a treacherous as the study of anything else, in that the scientist is prone to find things she can think of, and more rarely discovers things she did not suspect; she is also limited by the tools she has at her disposal. Most brain scientists who study dyslexia nowadays look at the function of the brain while the dyslexic is carrying out a language task.
For this, functional imaging with a magnetic resonance imager is used (like the one your physician uses to diagnose the cause of a headache, for instance, but used in a different way). First, the look is already biased, because language is emphasized (with rare exceptions in the field). Second, the look is biased, because it focuses on the function of the cerebral cortex (the highly folded rind containing most of the brain cells, or neurons, covering the cerebrum, which has grown out of proportion in human beings). It tends to miss the deeper parts of the brain, and misses the brainstem altogether, where more of sensory and perceptual experiences are processed.
There are clearly differences in the ways the brain functions when faced with a language task in dyslexics compared to good readers. For instance, the processing that should be mostly mediated by a given region of the cortex, is displaced both to other regions in the same hemisphere of the brain and to the other hemisphere, which means that the language circuits are altered. Areas that should be quiet during the task are not quiet, and those that should be highly activated are less activated, or not activated at all.
What do these differences mean?
We know that dyslexics read differently already. If the brain tests don’t show it, there is something wrong with the brain tests. Further, the tests have to go beyond showing differences which we already know exist. They have to tell us about mechanisms, the knowledge of which might help us with diagnosing dyslexia earlier, earlier at least than a child’s ability to read, even speak. This is because in dyslexia, as with other developmental cognitive conditions, early diagnosis promises better prevention and treatment. Another potential use of this kind of brain research would be to help us to differentiate among different types of dyslexia, presumably with different treatment approaches, which the reading tests alone may not be able to do. Finally, an altogether different type of scientist is looking for fundamental causes.
What are the genetic and environmental elements that predispose a child to dyslexia?
Some progress has been made in this regard, although I must say that progress has tangibly slowed down in the past couple of years. In order to discover a so-called dyslexia risk gene, it is important to examine literally thousands of people, and this presents a logistical problem for researchers. Some risk genes have been found and confirmed in more than one study (this is important). These genes, interestingly, point to pathways involved both in the structure and function of brain cells (neurons). They involve both neurons in the cerebral cortex and neurons in the deeper structures noted above. In some cases, the neurons may be noisy and unable to represent fine sound distinctions.
This is potentially very exciting, but still too early to make a great deal of. Potential outcomes of this research, if it pans out, would be medications that decrease the neuronal noisiness.
However, it should be stressed that the best therapy in this case would be to quiet down these neurons together with exposing the child to special education. It is not different from what I tell my patients with attention deficit disorder: “Look, this medicine will make your brain more suitable for learning in the classroom and while reading, but it won’t learn for you; you still have to study!
More is coming
There is a lot more about dyslexia research, and one of the most exciting parts of it is that it dovetails nicely with biological research on other learning and developmental disorders. So, there are lots of people working to make things better. Moreover, there are lots of people making sure that the research is good.
In the end, what we want to do is to diagnose the risk earlier and plug the young children into programs that will lessen the impact of whatever negative neurobiological burden they were born in, while at the same time spending more time developing their particular genius.
Professor Albert M. Galaburda is currently in Australia and will be presenting at the The Learning Difference Convention in Sydney on 6th & 7Th August at Rosehill Gardens Racecourse.
Professor Albert M. Galaburda Harvard University USA, is the Emily Fisher Landau Professor of Neurology and Neuroscience Harvard Medical School Co-Director of the Mind, Brain, and Behavior Interfaculty Initiative Harvard University Chief, Division of Cognitive Neurology.