Neurobiological defects

4.2 Neurobiological defects

Researchers thought already at the beginning of the 20^th century that dyslexia could be caused by some abnormalities in the brain functions of the dyslexics but it has not been until recently that new technological innovations have really shed some light on how the dyslexic brain actually works. In this chapter I will introduce the possible neurobiological caused behind dyslexia.

4.2.1 Defects of the visual processing and magnocellular deficit hypothesis

Majority of the researchers in the early 20^th century thought that dyslexia was mainly a visual disorder (Gayán Guardiola 2001, 7). Orton, for example, suggested in the 1930s that the cause of dyslexia might be the unclear dominance of the two hemispheres, which disturbs the restoration of visual memories (Poussu-Olli 1993, 25-26). He proposed that the mirror images of letters restored in the non-dominant hemisphere disturbed the visual processing and caused the letters to rotate (Korhonen 1995, 163). The visual deficits have since been studied a lot and there is evidence that a small group of dyslexics seem to have visual problems, such as poor vergence control and visual distortions (Ramus 2003, 3). What causes this is not entirely

clear. One explanation for these problems is offered by the recent magnocellular deficit hypothesis.

The magnocellular deficit hypothesis suggests that the magnocellular system, which controls eye movements and visual acuity and which is sensitive to rapidly changing, lower-frequency and moving information, functions defectively and more slowly on some dyslexics (Reid 2004, 11, Korhonen 2002, 157). This could explain the problems in reading accuracy and fluency as well as lower sensitivity to contrast that many dyslexics have (Reid 2004, 11;

Korhonen 2002, 157). Recently this hypothesis has been challenged by studies which claim that the visual deficits “cover the whole range of spatial and temporal frequencies” and it is thus probable that the visual difficulties are not related to magnocellular dysfunction at all but are a possible independent cause of reading disability (Ramus 2003, 3-4).

4.2.2 Differences of the hemispheres

Even though Orton's theory on the unclear dominance and the problems of visual processing did not prove to be the main cause of dyslexia the function of the hemispheres and its relation to dyslexia has been studied a lot since those days. Researchers have found out that the hemispheres of the dyslexics do differ from those of other people, and it has also been shown that even though the linguistic functions of the dyslexics, like those of other people, are usually situated in the left hemisphere, the difference between the hemispheres is not as clear on dyslexics (Korhonen 2002, 143). The researchers are not, however, sure whether this unclear dominance actually is the cause of dyslexia, like Orton thought, or whether it is the result of the disorder (Korhonen, 2002 143).

What has been discovered, however, is that the areas of the planum temporale in the back of the temporal lobes of the hemispheres are symmetric on dyslexics while on other people the left planum temporale, which is closely related to linguistic functions, tends to be bigger (Korhonen 2002, 141). Thus the symmetry of the hemispheres could be a cause for

dyslexia. Some scientists do not recognise this difference but state that the parietal areas of the brain of the dyslexics are exceptionally symmetrical and imply that the more symmetrical they are the more the person has difficulties in phonological processing, i.e. with the ability to perceive and restore phonemes and to operate with them (Korhonen 2002, 143). Some

researchers point out, however, that planum symmetry is not a very deciding factor in dyslexia to begin with as “structural asymmetries are distributed along a continuum of individual degrees” (Miles and Miles 1999, 85).

Despite the planum temporale areas brain research has also shown that the magnocellular areas of at least some dyslexics contain cells that are smaller and “more variable in size and shape” and it has been proposed that abnormalities in the probable auditory magnocellular system could cause the difficulties in “processing auditory

information at high speeds” and would thus be the cause for phonological difficulties (Miles and Miles 1999, 83-84). Ramus (2003, 2) offer a conflicting view as studies prove that auditory disorders “are restricted to a subset of the dyslexic population” and “it therefore seems that the phonological deficit …can arise in the absence of any auditory disorder”.

These abnormalities of the brain emerge already before the birth and during early infancy as the neuronal cells fail to connect correctly to the right areas of the brain causing the brain mechanisms to function and interact differently (Miles and Miles 1999, 82). Some studies suggest that these abnormalities in the brain development are caused by genetic factors (Poussu-Olli, 1993, 33, Galaburda 2005, 155) but some propose that environmental factors, such as biological, chemical or physical factors, that can occur prenatally, natally or postnatally may have an affect on the disorder as well (Ahvenainen and Holopainen 1999, 4).

For example, Hanna-Sofia Poussu-Olli states that the lack of oxygen or nutritional disorders during pregnancy may cause these abnormalities (Poussu-Olli, 1993, 160).

The abnormalities found in the brain of the dyslexics which could explain the difficulties in processing visual, auditory and phonological information are thus apparently

mainly caused by a mutation in genes which then disturbs the migration of the neuronal cells and causes them to connect incorrectly and the different parts of the brain function and interact defectively (Galaburda 2005, 161).

4.2.3 Differences in the brain functions

Besides differences in the anatomy of the brain it has also been shown that the brains of the dyslexics function differently. During the last few decades new technology has offered new views on the research on dyslexia. For example some EEG (electroencephalogram) tests have shown that the brain wave activity of the dyslexics differs significantly from that of other people (Korhonen 2002, 145). Also tests using the ERP-technology (event-related potential), which is used to show mismatch negativity (MMN) when the brain recognise a deviating stimulus for example in a series of sounds, have shown, for example, that dyslexics have a deviating MMN when the different sound stimulus is a part of a group of sounds but not when the sounds are presented as pairs (Korhonen, 2002 147). These results have been interpreted as showing that dyslexics have difficulties especially in auditive processing (Korhonen 2002, 147) and thus difficulties in distinguishing specific phonemes in words, which is further connected to defects in phonological processing.

Also PET (positron emission tomography), which measures the metabolic activity of the brain during specific tasks, and MRI (magnetic resonance imaging), which offers “very detailed images of brain and body tissue”, have brought new information on how the brain of the dyslexic actually works and how it differs from “normal” brain activity (Miles and Miles 1999, 84-85). MRI tests, for example, indicate that the left hemisphere posterior brain systems do not function correctly on dyslexics and thus they process visual motion abnormally (Lyon and Moats 2003, 4-5). Some researchers have proposed that this would refer to “a deficit in the magnocellular system” and thus support the disputed theory (Miles and Miles 1999, 87).

Studies using PET-scan have, on the other hand, revealed for example that during a task which requires phonological processing dyslexics activated the same areas of the brain as the control group but did not do so “in concert” (Paulesu et al. 1996, 150). And unlike the control group dyslexics did not activate the insula, which “has a major role in linking the different phonological codes”, at all, which according to Paulesu et al. (1996, 152, 154) could refer to a disconnection between anterior and posterior speech areas. The dyslexics also differed from the control group in a short-term memory task as they did not activate their right hemisphere at all (Paulesu 1996, 153). This evidence would propose that dyslexics might have some kind of a disconnection-syndrome as they fail to activate all the areas needed for phonological processing at the same time but are able to activate them separately (Paulesu at al. 1996, 154).

In general, it is thus a fact that dyslexic brain function differently. What causes this is still being debated. Paulesu et al. (1996, 154) suggest that the cause is a disconnection

between different phonological codes. Some, however, suggest the cause might be ‘general timing hypothesis’ because dyslexics have difficulties processing not only visual or

phonological incoming information but “fast incoming sensory information...in any domain”

(Miles and Miles 1999, 87).

4.2.4 Fatty acids

Biochemistry has also contributed to the research of dyslexia by offering a possible cause for the abnormal brain functions of dyslexics – the imbalance of fatty acids (Miles and Miles 1995, 86). Certain fatty acids “are known to be particularly important for visual and cognitive development” and a study showed that a dyslexic group did have an abnormal cerebral metabolism of phospholipids compared to the control group (Miles and Miles 1995, 87).

According to this it might be possible that a deficiency of some fatty acids could be “a contributory factor in dyslexia “ (Miles and Miles 1995, 87).