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Lower brain activity in visual cortex associated with dyslexia

A new study supports the idea that dyslexia may be caused by a subtle impairment of vision.

The study of a small group of dyslexics, performed by Stanford researchers and reported in the Nov. 25 issue of the Proceedings of the National Academy of Sciences, found that the level of brain activity in the visual cortex, the portion of the brain devoted to processing visual signals, appears to predict the speed at which people with dyslexia can read.

This is one of only a handful of cases in which a strong link between individual behavior and brain differences has been established.

"We found compelling evidence that there is a visual deficit associated with dyslexia, but at this time we don't know for certain if the deficit causes dyslexia or is just a marker for it," said David J. Heeger, assistant professor of psychology at Stanford. Heeger, postdoctoral student Geoffrey M. Boynton and graduate student Jonathan B. Demb (now a postdoctoral fellow at the University of Pennsylvania) co-authored the paper. inplane.GIF

The two images show the areas in the brain of dyslexics that were scanned using functional MRI. The scans show the activity taking place in a thin slice of the brain. The white line that runs diagonally through the side view of the skull shows the plane on which the readings were made. The top view of the brain shows the regions where activity was measured when the subjects were observing moving grids in high and low light levels. Subjects who had low levels of activity in the primary visual cortex, marked in blue, and in the MT region, noted in green, while watching moving grids in low light levels also proved to be slow readers. Reading speed is generally considered an indication of the severity of dyslexia in adults.


Since 1925 there has been interest in the possibility that dyslexia, which affects between 3 to 9 percent of the population, might be caused by a specialized type of visual impairment. Recently, this theory has been largely superseded by the view that the condition is caused by a disorder within the brain's language centers that interferes with an individual's ability to isolate and manipulate sounds.

The new results are too preliminary to affect the diagnosis or treatment of dyslexia, the researchers cautioned. But the study suggests a line of further research that could provide additional information about the relationship between visual system impairments and dyslexia. If future research should confirm the correlation between specific kinds of brain activity and dyslexia, it could lead to methods for diagnosing dyslexia at an earlier age than is now possible, the researchers said.

The Stanford researchers used a technique called functional magnetic resonance imaging (MRI) to measure differences in brain activity in dyslexics and non-dyslexics. MRI is a non-invasive way to study what is going on in the body. It relies on the fact that when the body is placed in an external magnetic field, its atomic nuclei absorb radio waves at certain precise wavelengths. Functional MRI is a special type of MRI that allows scientists to take pictures of the brain while people are thinking. It does so by remotely sensing the ratio of oxygen-rich and oxygen-depleted blood in different regions of the brain. This provides a map of neural activity because heightened activity increases the amount of oxygen-rich blood flowing to the region where it occurs.

The Stanford researchers were attracted to the problem of dyslexia by a study published in 1991 by Margaret Livingstone, Albert Galaburda and their colleagues at the Harvard Medical School. The Harvard researchers attached electrodes to the scalps of a group of dyslexics and non-dyslexics and claimed to find a difference in the electroencephalograms (EEGs) of the two groups when they were performing certain visual tasks. The researchers also did a post-mortem study of some people with this reading disability and found differences in their Lateral Geniculate Nucleus (LGN), a pea-sized part of the thalamus located in the middle of the brain.

Neurons that originate in the retina travel to the LGN before traveling to the back of the brain to connect at the primary visual cortex. From the primary visual cortex they fan out and make connections at a number of secondary locations in the back of the brain devoted to processing visual information. Some of these neurons are grouped together to form a pathway. One of these pathways, made up of large-sized neurons, is called the magnocellular, or M, pathway. Livingstone and Galaburda looked at the subdivision of the LGN that holds the cells in the M pathway and found that the cells are smaller in people with dyslexia compared to non-dyslexics.

These results led scientists to propose that a deficiency in the M cells could give rise to dyslexia. Animal studies suggest that the M pathway is involved in fast visual processing and the control of eye movements, suggesting that an M cell deficiency might cause dyslexia by making it difficult for people to recognize rapidly scanned print or by interfering with the fine motor control of the eyes required for reading.

Several behavioral studies have been conducted that have reinforced this hypothesis. The studies have demonstrated that dyslexics have extra difficulty in picking out visual patterns displayed at very low contrast. This implicates the M pathway because animal studies have shown that the M pathway also specializes in carrying low-contrast images.

This body of information inspired the Stanford researchers to design an experiment to test two predictions that should hold true if dyslexia results from a deficiency in the M pathway:

  • The degree of the deficiency of the M pathway should strongly correlate with the severity of the reading disorder;
  • Physiological differences should exist between dyslexics and non-dyslexics at the primary visual cortex or earlier in the visual pathway.

The researchers found 10 Stanford students ­ five dyslexics and five non-dyslexics to serve as controls ­ who agreed to participate in the experiment, which involved a total of nearly 60 hours of functional MRI imaging. The experiments were directed by radiology Professor Gary H. Glover and performed at the Stanford Medical Center in the Richard M. Lucas Center for Magnetic Resonance Imaging and Spectroscopy.

Using a technique developed by fellow psychology Professor Brian Wandell and Steve Engel (now an assistant professor at the University of California-Los Angeles) that allows researchers to identify early vision centers, the researchers were able to locate the primary visual cortex in all of their subjects.

Because of the LGN's location, it is very difficult to use functional MRI to measure activity levels within it. However, animal studies have shown that a secondary region called MT+ is dominated by M pathway input. So the researchers decided to use activity in this region as a proxy for the activity in the M pathway. Using another technique they successfully located the MT+ region in all their subjects.

The researchers exposed their subjects to two sets of visual stimuli: moving grids displayed at low and high light levels. As they watched these patterns, the subjects' brain activity levels in the primary visual cortex and MT+ locations were recorded.

Last year, while the Stanford researchers were in the middle of their experiment, a group of National Institutes of Health researchers headed by Guinevere Eden (now at Georgetown University Medical Center) published the results of a somewhat similar study. Eden's group used functional MRI to establish that there is a gross difference in the activity levels of the MT+ area between dyslexics and non-dyslexics: When subjects were shown moving patterns, activity in the MT+ region of non-dyslexics was easy to spot, but the activity level among dyslexics was below the experiment's observational threshold and so was undetectable, the NIH scientists reported.

By successfully measuring the neural activity in the MT+ regions of the brains of their dyslexic subjects, as well as in that of the non-dyslexic controls, the Stanford researchers were able to take a major step beyond the Georgetown study. When they compared the levels of brain activity in the MT+ location of the five dyslexics with their respective reading speeds they found an unexpectedly strong correlation: Lower activity levels were associated with slower reading speeds. Reading speed is generally considered to be the best general measure of the severity of dyslexia in adults.

The researchers also found a weaker but still positive correlation between activity in the primary visual cortex and reading speed, which provides additional support for the hypothesis that the underlying problem lies in the visual system at or before the visual cortex.

These results are fully consistent with the proposition that dyslexia is caused by impairment of the M pathway. It is possible, however, that dyslexics might have similar deficiencies in their ability to handle fast temporal signals in other important sensory pathways as well. In that case their reading problems could be caused by a different manifestation of this condition. But it is difficult to imagine that such an abnormality in a significant visual pathway would not have some effect on a visually complex behavior like reading, the researchers have concluded.

This is one of only a handful of studies (performed by other research groups) that have found strong links between individual behavior and brain differences. One such study, for example, found that subjects with greater brain activity in a specific area in the right hemisphere, called the amygdaloid complex, were better able to remember emotional information. Another study found that activity in the left medial temporal lobe was correlated with an individual's ability to remember word lists. A third study established that subjects who were better at forming mental images did so with lower levels of brain activity.

The Stanford research was funded by Stanford's Office of Technology Licensing, the Stanford Graduate Research Opportunities Fund, the Sloan Foundation, the Orton Dyslexia Society, the National Institutes of Health and the National Institute of Mental Health.


By David F. Salisbury

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