Dyslexia is a defined as a learning disability characterized by problems in expressive or receptive, oral or written language. Derived from the Greek words "dys" (poor or inadequate) and "lexis" (words or language), dyslexia and other learning disabilities affect about 15% of the population. (What is dyslexia!) Dyslexia itself can manifest itself in many different ways. People with dyslexia do not see words "backwards" or have other vision problems. Many dyslexics are gifted with outstanding musical abilities, or the ability to solve three-dimensional puzzles with little difficulty. (What is dyslexia!) It is not representative of a below average mind and is not caused by behavioral or social problems. Dyslexia is caused by differences in the function and structure of certain areas of the brain. (What is dyslexia!) Because of this, Dyslexia can not be cured and will never be outgrown. Appropriate teaching methods are taught to help those with dyslexia overcome their weakness by using their strengths. Understanding how this disability works and where it stems from can only help in the search for beneficial teaching techniques.
Because there are many different aspects of dyslexia, very few dyslexics show all the signs of the disorder. Understanding some of the more devastating symptoms of the disorder provide a strong base for research in the area. Dyslexics may have difficulty encoding words, not be able to recognize sequences of numbers or of letters in words, either when read or written, or not be able to fully interpret instructions that they have been given. Imagine a person driving down the road who cannot distinguish between a sign that says 15 mph and 51 mph. Or a person who cannot follow instructions to give CPR or some other life saving technique. Although these may seem frivolous or inconsequential, the main effect of this learning disorder is that it impairs the intake and processing of information that can eventually greatly effect that person’s life.
Because of the lifelong effects of dyslexia, much study has been conducted to determine the cause and best treatment of the disorder. A study conducted at Harvard in 1984 proposed that dyslexia was a normal variation in the human brain (due to evolution) and therefore was not a disorder. (Newman, 1998) This theory was based on a supposed enlargement of the right side of the brain, the side that deals with spatial perception, faces, art, and music, and a decrease in growth on the left side of the brain (Broca area) which deals with the primary language processing. (Newman, 1998) Dyslexics with extraordinary musical, engineering, artistic, or intellectual talents provide support for this theory. Explanation of this theory is included in this report to show how far along research into dyslexia has progressed.
Initial research into the role of magnocellular cells in dyslexia was brought about by Dr. Livingstone at Harvard University in 1991. It was proposed that when you read, light strikes the photoreceptors in the retina, from which information is processed in the midbrain by the magno and parvo cells. After the information passes through these two types of cells, it moves to the visual cortex for further processing. This major pathway is slowed down by an abnormality in the dyslexic mind, causing the two kinds of visual information to be presented in the improper sequence. (Newman, 1998) This and many studies afterwards have helped show that 75% of dyslexics have defects in their main magnocellular pathways. Although the evidence in favor of this theory is abundant, there have been some studies that did not get the same results. A study conducted in 1995 measured contrast sensitivity for low and high spatial frequency targets at several stimulus durations. The dyslexic subjects were less sensitive at the higher frequencies, but showed no difference between regular participants at lower frequencies. (Newman, 1998) Sampling bias is a suggested reason for these results, because only 75% of people with reading disorders suffer from deficits in magnocellular pathways, the studies could have used participants from the latter 25%. For whatever reason, these results are not consistent with a deficit in the magnocellular pathway.
According to E. Borsting (1996), dyslexia has been identified with three different subtypes: dyseidesia, dysphonesia, and dysphoneidesia. Dyseidesia is a deficit in the ability to perceive whole words with their sounds. This mainly effects the reading of non-phonetically regular words, such as laugh. Dysphonesia is a deficit in word analysis skills. These people have trouble with unfamiliar words as well as word association, as in the difference between home and house. Dysphonedeisia is a combination of the previous two. Neurological studies show that each subtype affects a different area of the brain, giving support to the 75% theory of magnocellular deficits. (Borsting, 1996)
Other recent research by P.L. Cornelissen shows that children with reading disabilities have more difficulty detecting flickering or moving visual stimuli. This research is consistent with the magnocellular deficit theory, causing misrepresentation of where letters are positioned in correspondence with each other. It has been shown that there is a positive relationship between children’s motion detection thresholds and the likelihood of them making a letter recognition error. However, phonological factors were also found to have an effect on explaining the children’s errors. (Cornelissen, 1998)
Research into this topic is constantly being conducted. Until we can pinpoint the main causes of all forms of dyslexia, we will not be able to fully understand and deal with its effects. The existing data on the magnocellular deficit theory is still somewhat conflicting. Because of this conflicting data, one suggestion for further research would be to investigate the reason behind these differing results. According to Skottun, Borsting has shown that magnocellular deficits may be linked to only one sub-type of dyslexia, while Cornelissen shows contrast sensitivity loss to occur at low but not high luminance levels. Learning not only what causes dyslexia, but also what causes experimental discrepancies, is the key understanding and conducting research to aid in the battle against these learning disabilities. (Skottun, 1997)
References
Borsting, E. (1996). The presence of magnocellular defect depends on the type of dyslexia. Vision Research Issue 36, 1047-1053
Busey, T. (1997). The temporal frequencies underlying localization and character identification. [Online]. Abstract available: http://cognitrn.psych.indiana.edu/busey/idloc/idloc.html
Cornelissen, P.L. (1998). Coherent motion detection and letter position encoding. Vision Research Issue 38, 2181-2191.
Cornelissen, P.L. (1998). Magnocellular visual function and children’s single word reading. Vision Research Issue 38, 471-482.
Newman, Renee (1998, April). Dyslexia: Explanations from science. [ 8 paragraphs.] Dyslexia and Dyscalculia Support Services of Shiawassee County available: http://www.shianet.org/~reneenew/dysl.html
Ridder, W.H. 3rd (1997). Not all dyslexics are created equal. Optometry and Visual Sciences, 74 (3), 99-104.
Skottun, B. C. (1997). Some remarks on the magnocellular deficient theory of dyslexia. Vision Research Issue 37, 965-966.
What is Dyslexia!. [3 paragraphs]. Discover Technology [Online]. Available: http://discovertechnology.com/whatisdyslexia.html
Report by:
Timothy Ballew