Anna Mallach delves into efforts to understand dyslexia and asks what still needs to be done
Reading and writing are complex human behaviours, which have only recently gained importance from an evolutionary point of view. Whilst we have always relied on our senses to see, feel, hear and taste the world around us, only with the advent of mass printing did reading become an essential component of our lives.
According to research at Stanford University, 5-17% of the population suffer from dyslexia, defined as a deficit in reading and writing abilities, independent of other mental abilities and motivation. Dyslexia is often diagnosed first in children beginning to fall behind their classmates with their reading ability. Associated symptoms of this disorder can also concern oral language, motor movements and clumsiness. But the key questions are, why do some children develop this disorder? And how could we understand the neuroscience behind it?
Studies have suggested that there is a genetic component to dyslexia, with children from a familial background of dyslexia having a 50% risk of developing the disorder as well. Some candidate genes have recently been identified, which may shed a little light on its neuronal basis.
Our brain is formed from two highly sophisticated cerebral hemispheres, which share the brain’s tasks. For the majority of people, the left hemisphere is heavily involved in processing language. The suggested dyslexia risk genes, such as ROBO1, DCDC2 and DYX1C1, seem to play a role in the migration of neurons to the future language centres in the left hemisphere. If the migration of neurons to these regions is disrupted, this may impair the ability to process language, resulting in symptoms of dyslexia.
In addition to neuronal migration, there are a number of theories linking neural processes with reading and writing impairments. For example, dyslexic children often have problems differentiating between visually similar letters such as “m” and “n”, suggesting deficits in visual processing. Further, some areas of the brain involved in seeing and making sense of the world outside are less active, effectively meaning that letters appear to blend into each other.
However, differences in the visual system between dyslexic and unaffected children are difficult to interpret. Learning to read modulates our brain, leading to letters being processed in the brain’s language centres rather than simply as images. Reduced reading abilities, as seen in dyslexic children, could lead to different visual development compared to unaffected children. Therefore, when examining children with dyslexia, it is difficult to differentiate between the effects that problems with the visual system have on reading, and in turn, the effect that reading abilities have on visual development.
It’s also possible that processing rapid stimuli, independent of whether they are auditory or visual, can be challenging for dyslexic children. Some brain areas are better at keeping track of stimuli which change quickly, such as scanning letters on a page, one of which is theorised to be the left hemisphere. As previously mentioned, the left hemisphere appears to also display reduced processing power in dyslexic children, affecting the ability to process these stimuli. Thus, the combination of deficits in tracking rapid stimuli and reduced processing in language areas means that understanding spoken or written language gets even harder.
By far the most prominent theory, however, is the phonological theory: difficulties may arise from a perceptual deficit, such as a more elementary auditory problem. When children learn how to speak, an important aspect to learn is that spoken language can be broken down into small units of sound, known as phonemes. These sounds can be represented by letters or syllables, forming written language. However, researchers have found that children at risk of developing dyslexia have problems working with phonemes, leading to problems manipulating them in an abstract way .
Yet, interestingly, dyslexia can be found across all cultures. Even in the Chinese-speaking world, who use a logographic language where the smallest written units convey meaning rather than sound, the prevalence of dyslexia is the same as that in phonemic languages. This suggests that phonological deficits are probably not sufficient to cause dyslexia.
The most common treatments for dyslexia are based on intensive instruction of oral language skills and phonological processing. It has been found that the earlier the treatment is applied, the more likely the child is to achieve average reading abilities. Following treatment, language centres in the left hemisphere have increased activity, which correlates with oral language improvement.
Overall, the general problem with studying dyslexia and discerning its effects on neuronal functioning is the influence dyslexia may have on cognitive development. Children with dyslexia have reduced reading abilities, have probably experienced frustration when trying to read, and may have been individually worked with as part of their treatment. This makes it difficult to determine whether the differences seen between dyslexic and normal children are because of a possible causes of dyslexia, or the effect dyslexia itself has on the developing brain of the children.
Until we better understand dyslexia, UCL is providing support for dyslexic students. You can find more information at: http://www.ucl.ac.uk/disability/who-we-support/dyslexia
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