Most research into in function and brain anatomy in people who are deaf has involved deaf and hearing signers, and hearing non-signers. Because the majority of individuals who are deaf are born to hearing parents and therefore use English or another spoken language as their first language, we asked whether conclusions drawn about the effects of sensory experience in native users of sign language would hold when studying deaf and hearing subjects who are not native users of sign, but native users of English (i.e. they consider English their first language).
In a paper published in the Journal of Neuroscience (Olulade et al., 2014) we studied deaf and hearing native users of American Sign Language and deaf and hearing native users of English. We acquired anatomical data with MRI and examined differences in gray matter and white matter. We found that deaf and hearing participants, irrespective of language experience, differed in the volume of brain white matter in their auditory cortex. But, we also found differences in left hemisphere language areas that were specific to the group of participants who are deaf whose native language was ASL. This means that observations on brain anatomy that have been attributed to sensory experience are in some instances dependent on the native language experience of that person. Our findings demonstrate that restricting investigations of brain structure and function to native users of ASL means that the results cannot be generalized to all deaf people. We are now continuing this line of investigation with functional brain imaging data acquired during a visual task.
Developmental dyslexia is a reading disability that occurs in about 7 to 12% of the population. Using brain imaging technology (magnetic resonance imaging or MRI), previous studies of dyslexia have found less brain tissue volume, specifically gray matter, which is the brain tissue that houses the connections of nerve fibers. The locations of the differences where dyslexics differed from non-dyslexics are in regions of the brain involved in language, reading and skills known to support reading such as phonological awareness, consistent with the long-held view that dyslexia is a language-based learning disability. Here, we expanded on these anatomic studies by not only comparing dyslexic children to their age-matched peers, but also to a group of typical readers who were younger than the children with dyslexia but read at the same level. This second group allowed us to ask the question of whether the anatomical differences previously observed in studies of dyslexia represent a cause of reading disability or rather a consequence of the lesser reading experience.
When the children with dyslexia were compared to typical readers of the same age, we found results similar to those previously reported. Namely, less gray matter volume in a left hemisphere posterior temporal region as well as other locations. However, when the same children with dyslexia were compared with the younger children who read at the same level, this difference in gray matter volume was not found. Because the anatomical difference was only observed when the typical readers were of the same age, it suggests that this gray matter volume difference may in part be a result of the difference in reading ability as opposed to the actual cause of reading problems.
Brain Anatomy of Dyslexia Is Not the Same in Men and Women, Boys and Girls
This study, published in Brain Structure and Function in 2013, is the first to examine anatomical differences, specifically gray matter volume, in the brains of females with and without the common reading disability developmental dyslexia. Read more...
Previous studies of brain anatomy in dyslexia have been confined to all-male or male-dominated samples because the prevalence of dyslexia is 2 to 3 times higher in males than in females; yet the results have been generalized to all people with dyslexia, male and female. In this new study, involving a total of 118 participants, when men with and without dyslexia were contrasted with non-dyslexics, anatomical differences were seen in temporal-parietal cortex, consistent with prior reports. However, the novel parallel comparison of women with and without dyslexia revealed differences not in brain regions associated with language function, but instead in areas that control sensory and motor function. Sex-specific differences in dyslexia were seen not only in adults, but also in children, suggesting that females with dyslexia have their own unique neuroanatomical differences across the lifespan.
Our results raise important questions about whether the etiology of dyslexia is different in males and females and suggest that researchers and practitioners need to consider female dyslexics as a group separate from male dyslexics.
Abnormal Visual Motion Processing is a Consequence and not a Cause of Developmental Dyslexia
There is a long-standing debate about whether the visual symptoms observed in developmental dyslexia (attributed to dysfunction of the visual magnocellular system and measured here via brain activity underlying visual motion perception) have a causal role in this common learning disability. In this study, published in Neuron in 2013, we found a correlation between magnocellular visual system function and reading ability in normal controls. Read more and see our Video Abstract of the study (5 minutes)
We also found a weakness in magnocellular visual system function in dyslexia (as reported in our Nature paper in 1996). However, we provide two types of new evidence that dyslexia is not caused by this magnocellular deficit as has been widely claimed.
First we show that when dyslexic children are compared to younger children matched on reading ability ("reading-level-matched design"), there is no longer a difference between dyslexics and controls, questioning the causality of visual system differences. Secondly, following a language-based reading intervention program, brain activity in the magnocellular system is coupled with reading gains in the dyslexics.
These data demonstrate that the visual magnocellular deficits observed in dyslexia are not the cause of dyslexia. Further, they counter the hypothesis that magnocellular problems are a symptom of dyslexia per se (i.e., co-existing with the language-based problems that drive the reading deficits); rather, they are the consequence of not learning to read, because learning to read mobilizes the visual magnocellular system.
Finally, our observation that gains in reading are followed by changes in brain regions subserving visual motion perception makes an important and independent contribution to a small body of work that has begun to demonstrate that the culturally-imposed process of learning to read results in experience-dependent plasticity in brain areas outside of the reading network.