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Florida Learning Disabilities Research Center



Debunking the Magnocellular Deficit Theory of Dyslexia

By: Mia Daucourt

Dyslexia is a common reading disability in which a person does not read as well as you would expect them to, based on how old they are, how smart they are, and the opportunities they have had. Thus, compared to their other abilities, their reading is unexpectedly deficient. A dyslexic reader tends to take longer to read the same amount of reading material and to have to re-read many words multiple times compared to non-dyslexic readers. Many years of research have shown that one of the most common causes for this reading deficiency is a problem with being able to match up written letters and words to their corresponding speech sounds. This shows up as less fluent, or slower reading, which characterizes dyslexia. However, this problem with matching up letters and sounds, which we call a “phonological deficit” is not found in every dyslexic reader, showing that dyslexia has more than just a single cause.

Another proposed single cause of dyslexia is a “magnocellular deficit.” Our visual system is comprised of three different layers, each of which serves a distinct purpose for processing visual information. The magnocellular layer is specialized for quick, in-the-moment responses to visual information involving motion, location, and timing. It guides visual attention and timing and directs our attentional spotlight when reading. The attentional spotlight is what allows our visual system to focus on the right location within a word or phrase while reading. Some researchers propose that the issues the magnocellular system creates with eye movement control, impeding a reader’s ability to keep their attention on visual information, and creating peripheral vision deficits are all likely to be detrimental to an individual’s ability to read, and are especially likely to make it hard for an individual to read quickly. However, some evidence has not matched up with this magnocellular deficit hypothesis, suggesting these issues with the magnocellular vision stream are not the reason we find differences between dyslexic and non-dyslexic readers. Furthermore, like the phonological deficit hypothesis, the magnocellular deficit is not found in every dyslexic reader, and not every person with a magnocellular deficit has dyslexia, showing that there are probably many other reasons that dyslexia exists.

In order to figure out how a magnocellular deficit and dyslexia are related, Edwards & Schatschneider (2019) at Florida State University conducted an experiment with 83 undergraduate students to test the links between the magnocellular system and reading performance using a series of reading tasks. Since the role of the magnocellular layer of the visual system is to process visual information quickly, the researchers focused on timed reading performance, or reading fluency, which captures both the accuracy and speed in a persons’ reading ability measured as words per minute. As I previously mentioned, dyslexic readers have a problem with their reading rate and tend to read more slowly than non-dyslexic readers, so reading fluency is the best way to tap into these reading deficits directly. They tested reading fluency in two different formats, one in which the undergraduate participants read out loud (oral reading fluency) and another in which they read silently, in their heads (silent reading fluency).

The researchers also investigated whether the role of a magnocellular deficit in dyslexia may be related to the magnocellular system’s control of a person’s attentional spotlight by giving the undergraduates two different letter naming fluency tasks, one that involved reading a grid of consecutive letters (rapid automatic naming or “RAN”) and another task that required them to name one letter at a time (isolated naming) as quickly and accurately as possible. They figured that the isolated naming task would be easier than the RAN task because it’s easier to focus your visual attention on a single letter on a screen in front of you than it is to read several letters in a row, which would require a well-functioning attentional spotlight in order to focus on the right letter at the right time.

Finally, the researchers assessed the functioning of each participant’s magnocellular system using two tasks, a flicker detection task and a coherent motion task. In the flicker detection task circles were presented on a computer screen and either made to blink on and off or not. Then, participants were asked to report whether or not they detected a flicker (aka, blinking) and given feedback on their accuracy each time. For the coherent motion task, 150 moving dots were presented on a computer screen, with a portion of the dots moving together either to the left or right of the screen. Then, participants were required to report whether the group of dots that was moving in unison was moving to the right or left of the screen, and they were given feedback on their accuracy each time. Both of these magnocellular tasks were scored based on accuracy, with participants who were more accurate in detecting flickers and coherent motion considered to have better magnocellular performance than participants who were less accurate.

Overall, the researchers found that the expected association between magnocellular task performance and reading fluency performance was not even there. Instead of participants with better magnocellular performance also having better reading performance than participants with poor magnocellular performance, the two skills were not significantly related, debunking the magnocellular deficit hypothesis. Based on these results, we can conclude that although the visual system’s magnocellular layer is likely to be important for reading performance, it is not the main driving force behind dyslexia. In light of the results of previous studies that found a significant positive association between magnocellular performance and dyslexia, the results of this study highlight the need for future dyslexia research to focus on multiple factors, instead of crediting dyslexia to a single origin. As we continue to make strides in treating dyslexia, we need to stop focusing on a single deficit hypothesis and instead look at the many contributing factors to reading performance.

Citation: Edwards, A. A., & Schatschneider, C. S. (2019). Magnocellular pathway and reading rate: An equivalence test analysis. Scientific Studies of Reading. doi: 10.1080/10888438.2019.1663856