Dyslexia is a defined as a learning disability characterizedby 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 otherlearning disabilities affect about 15% of the population. (Whatis dyslexia!) Dyslexia itself can manifest itself in manydifferent ways. People with dyslexia do not see words"backwards" or have other vision problems. Manydyslexics are gifted with outstanding musical abilities, or theability to solve three-dimensional puzzles with littledifficulty. (What is dyslexia!) It is not representative of abelow average mind and is not caused by behavioral or socialproblems. Dyslexia is caused by differences in the function andstructure of certain areas of the brain. (What is dyslexia!)Because of this, Dyslexia can not be cured and will never beoutgrown. Appropriate teaching methods are taught to help thosewith dyslexia overcome their weakness by using their strengths.Understanding how this disability works and where it stems fromcan only help in the search for beneficial teaching techniques.

Because there are many different aspects of dyslexia, very fewdyslexics show all the signs of the disorder. Understanding someof the more devastating symptoms of the disorder provide a strongbase for research in the area. Dyslexics may have difficultyencoding words, not be able to recognize sequences of numbers orof letters in words, either when read or written, or not be ableto fully interpret instructions that they have been given.Imagine a person driving down the road who cannot distinguishbetween a sign that says 15 mph and 51 mph. Or a person whocannot follow instructions to give CPR or some other life savingtechnique. Although these may seem frivolous or inconsequential,the main effect of this learning disorder is that it impairs theintake and processing of information that can eventually greatlyeffect that person’s life.

Because of the lifelong effects of dyslexia, much study hasbeen conducted to determine the cause and best treatment of thedisorder. A study conducted at Harvard in 1984 proposed thatdyslexia was a normal variation in the human brain (due toevolution) and therefore was not a disorder. (Newman, 1998) Thistheory was based on a supposed enlargement of the right side ofthe brain, the side that deals with spatial perception, faces,art, and music, and a decrease in growth on the left side of thebrain (Broca area) which deals with the primary languageprocessing. (Newman, 1998) Dyslexics with extraordinary musical,engineering, artistic, or intellectual talents provide supportfor this theory. Explanation of this theory is included in thisreport to show how far along research into dyslexia hasprogressed.

Initial research into the role of magnocellular cells indyslexia was brought about by Dr. Livingstone at HarvardUniversity in 1991. It was proposed that when you read, lightstrikes the photoreceptors in the retina, from which informationis processed in the midbrain by the magno and parvo cells. Afterthe information passes through these two types of cells, it movesto the visual cortex for further processing. This major pathwayis slowed down by an abnormality in the dyslexic mind, causingthe two kinds of visual information to be presented in theimproper sequence. (Newman, 1998) This and many studiesafterwards have helped show that 75% of dyslexics have defects intheir main magnocellular pathways. Although the evidence in favorof this theory is abundant, there have been some studies that didnot get the same results. A study conducted in 1995 measuredcontrast sensitivity for low and high spatial frequency targetsat several stimulus durations. The dyslexic subjects were lesssensitive at the higher frequencies, but showed no differencebetween regular participants at lower frequencies. (Newman, 1998)Sampling bias is a suggested reason for these results, becauseonly 75% of people with reading disorders suffer from deficits inmagnocellular pathways, the studies could have used participantsfrom the latter 25%. For whatever reason, these results are notconsistent with a deficit in the magnocellular pathway.

According to E. Borsting (1996), dyslexia has been identifiedwith three different subtypes: dyseidesia, dysphonesia, anddysphoneidesia. Dyseidesia is a deficit in the ability toperceive whole words with their sounds. This mainly effects thereading of non-phonetically regular words, such as laugh.Dysphonesia is a deficit in word analysis skills. These peoplehave trouble with unfamiliar words as well as word association,as in the difference between home and house. Dysphonedeisia is acombination of the previous two. Neurological studies show thateach subtype affects a different area of the brain, givingsupport to the 75% theory of magnocellular deficits. (Borsting,1996)

Other recent research by P.L. Cornelissen shows that childrenwith reading disabilities have more difficulty detectingflickering or moving visual stimuli. This research is consistentwith the magnocellular deficit theory, causing misrepresentationof where letters are positioned in correspondence with eachother. It has been shown that there is a positive relationshipbetween children’s motion detection thresholds and thelikelihood of them making a letter recognition error. However,phonological factors were also found to have an effect onexplaining the children’s errors. (Cornelissen, 1998)

Research into this topic is constantly being conducted. Untilwe can pinpoint the main causes of all forms of dyslexia, we willnot be able to fully understand and deal with its effects. Theexisting data on the magnocellular deficit theory is stillsomewhat conflicting. Because of this conflicting data, onesuggestion for further research would be to investigate thereason behind these differing results. According to Skottun,Borsting has shown that magnocellular deficits may be linked toonly one sub-type of dyslexia, while Cornelissen shows contrastsensitivity loss to occur at low but not high luminance levels.Learning not only what causes dyslexia, but also what causesexperimental discrepancies, is the key understanding andconducting research to aid in the battle against these learningdisabilities. (Skottun, 1997)


Borsting, E. (1996). The presence of magnocellular defectdepends on the type of dyslexia. Vision Research Issue 36,1047-1053

Busey, T. (1997). The temporal frequencies underlyinglocalization and character identification. [Online]. Abstractavailable: http://cognitrn.psych.indiana.edu/busey/idloc/idloc.html

Cornelissen, P.L. (1998). Coherent motion detection and letterposition encoding. Vision Research Issue 38, 2181-2191.

Cornelissen, P.L. (1998). Magnocellular visual function andchildren’s single word reading. Vision Research Issue 38,471-482.

Newman, Renee (1998, April). Dyslexia: Explanations fromscience. [ 8 paragraphs.] Dyslexia and Dyscalculia SupportServices of Shiawassee County available: http://www.shianet.org/~reneenew/dysl.html

Ridder, W.H. 3rd (1997). Not all dyslexics arecreated equal. Optometry and Visual Sciences, 74 (3),99-104.

Skottun, B. C. (1997). Some remarks on the magnocellulardeficient 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