Developmental Learning Disability

About three decades ago, I was listening to Norman Geschwind speak about dyslexia to members of the Orton (dyslexia) Society. Norman liked to say things that would shock his audience, and during his talk he said, "Dyslexia is a social disease." At that time when someone spoke about social diseases, they were usually speaking about sexually transmitted diseases, such as gonorrhea and syphilis. There were many dyslexic people and parents of dyslexic children in the audience who appeared to be angry when he made this comment. He, however, held up his hand and said, "Wait, let me explain." He mentioned that in the history of humans, it is only recently that reading has become so critical for success. He asked who would be our leader if we lived in a hunter-gatherer society: the person who could read and write the best or the person who could get us back to camp after the hunt? He also mentioned that he would not be surprised if the people with the best visual-spatial abilities have a higher incidence of dyslexia.

Earlier I mentioned that Diamond et al. (1985) studied Einstein's left inferior parietal lobe, including Brodmann's area 39 or the angular gyrus (see Figure 3.5). When Diamond and coworkers performed a histological analysis of this area, they found that, compared with the brains of control participants, the angular gyrus (Brodmann's area 39) on the left side of Einstein's brain contained a higher glial cell-to-neuron ratio. These investigators attempted to explain this result by suggesting that this aberrant ratio was "a response by glial cells to greater neuronal metabolic need." They also suggested that this increased metabolic need might be related to Einstein's unusual conceptual powers. The report of Diamond et al. (1985) was severely criticized because with aging there is a loss of cortical neurons, and their control participants were younger than Einstein (Hines, 1998). These investigators provided no information about the control participants' socioeconomic status, their cause of death, or their premorbid health. Even if one assumes that methodological errors did not account for the results reported by Diamond et al., it is not apparent how a relative reduction of neurons could account for Einstein's creativity.

Einstein had developmental language disorders. Hoffman and Dukas (1972) quoted a part of a letter he wrote in 1954 where he explained, "My parents were worried because I started to talk comparatively late, and they consulted a doctor because of it. I cannot tell how old I was at that time, but certainly not younger than three." Like many children with delayed speech, Einstein also had developmental dyslexia (Kantha, 1992). Dejerine (1891) demonstrated that lesions of the left angular gyrus (Brodmann's area 39) induce acquired alexia, and it is possible that people with developmental dyslexia may also have abnormalities in this region. Kantha (1992) suggested that the abnormalities reported by Diamond et al. might have been related to Einstein's dyslexia rather than his genius. Geschwind and Galaburda (1985) suggested that the delay in development of the left hemisphere might allow the right hemisphere, which mediates spatial computations, to become highly specialized.

Einstein was perhaps the greatest scientist of the 20th century, and Picasso was one of the greatest artists. Picasso also appears to have had a language learning disability. Both of these individuals' creativity, in part, depended on spatial skills. Is this just a chance relationship or is there a significant relationship between developmental language disorders and the types of creativity that depend on visual-spatial skills? Unfortunately, there are still not many studies that have systematically examined this relationship. Wolff and Lundberg (2002) assessed art students at very a competitive university and compared them with other students at the university who were not art students. They found that the reported incidence of dyslexia was greater in the art students than in those who were not art students. Many develop-mentally dyslexic people have as their underlying deficit impaired phonological skills such that they have trouble converting letters or combinations of letters, such as the th (graphemes), into their associated speech sounds or phonemes. These investigators also assessed the art and nonart students' phonological skills and found that the art students' skills were significantly poorer than were those of the nonart students. Similarly, Eisen (1989) assessed the creative ability of children with and without learning disabilities. Eisen found that the children with learning disabilities performed better than the children without learning disabilities on the nonverbal task, but not on the verbal task. Winner and coworkers (2001), however, could not replicate these findings. Children with dyslexia often have other behavioral disorders, such as attention deficit disorder with or without hyperac-tivity, and although these disorders might have influenced the results of these types of experiments, the authors attempted to correct for these comorbid disorders, but still did not find that the dyslexic group had superior spatial skills. Hence, the relationship between developmental language disorders and spatial skills remains unresolved.

If we assume that people with developmental language disorders have greater spatial skills, what could be the explanation? As I mentioned earlier, in primates, including people, visual stimuli that come from the retina go to the occipital (visual) cortex by way of a relay station in the middle of the brain called either the optic thalamus or the lateral (visual) geniculate nucleus (see Figure 6.3). Visual information carried to the visual cortex may travel over a rapid transport system that has large cells in the optic thalamus and is thus called the magnocellular division. Alternatively, visual information might be transported by a slow transport system that has smaller neurons in the thalamus and is called the parvocellular division. Galaburda and Livingstone (1993) found that when they measured the speed of visual signals in dyslexic people, the dyslexic people's signals appeared to be slower than control subjects' signals, suggesting that visual information in these dyslexic people's brains was carried primarily by the slow or parvocellular system. When they studied the brains of people who were dyslexic and had died, they found abnormalities in the magnocellular system. The fast magnocellular system carries low-contrast information and the slow parvocellular system carries the high-contrast information. Reading letters and words would seem to depend more heavily on the high-contrast (parvocellular) system, and thus this finding in the visual system can easily explain dyslexia. The auditory systems, however, also have two parallel systems (parvocel-lular and magnocellular), and to be able to detect individual phonemes that make up words, a person has to perform a rapid auditory analysis. When children learn to read, they primarily use a grapheme (letter or letters) to phoneme (letter sound) conversion strategy to sound out words, and people who are unaware of the phonological composition of words often suffer with developmental dyslexia. Thus, a deficit in the magnocellular auditory system might preclude people from fully decoding the phonemic structure of words, and this might lead to developmental language disorders. In the visual system, whereas the parvocellular visual system is important in detecting what, the magnocellular division primarily is important in spatial processing. The findings that spatial skills are more dependent on the low-contrast, rapid transmission magnocellular system and that developmental dyslexic people have impairment in the magnocellular system would appear contradictory. Therefore, the observation that dyslexic people have superior spatial skills cannot be explained by this magnocellular deficit. If it is true that developmentally dyslexic people do have enhanced spatial skills, there would have to be another explanation, but I do not know what it is, unless developmental dyslexia in unrelated deficits in the magnocellular division and the disinhibition postulate I previously mentioned also accounts for these observations such that delayed development of the left-hemisphere reading-writing systems allowed the right-hemisphere visual-spatial and global-attentional systems to better develop.

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Adult Dyslexia

Adult Dyslexia

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