The majority of currently available dyslexia research relates to the alphabetic writing system, and especially to languages of European origin. However, substantial research is also available regarding dyslexia for speakers of Arabic, Chinese, and Hebrew.
In the area of neurological research into dyslexia, modern neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) have produced clear evidence of structural differences in the brains of children with reading difficulties. It has been found that people with dyslexia have a deficit in parts of the left hemisphere of the brain involved in reading, which includes the inferior frontal gyrus, inferior parietal lobule, and middle and ventral temporal cortex.
Brain activation studies using PET to study language have produced a breakthrough in understanding of the neural basis of language over the past decade. A neural basis for the visual lexicon and for auditory verbal short-term memory components have been proposed, with some implication that the observed neural manifestation of developmental dyslexia is task-specific (i.e., functional rather than structural).
fMRI’s in dyslexics have provided important data supporting the interactive role of the cerebellum and cerebral cortex as well as other brain structures.
Genetic research into dyslexia has its roots in the examination of post-autopsy brains of people with dyslexia. When they observed anatomical differences in the language center in a dyslexic brain, they showed microscopic cortical malformations known as ectopias and more rarely vascular micro-malformations, and in some instances these cortical malformations appeared as a microgyrus. These studies and those of Cohen et al. 1989 suggested abnormal cortical development which was presumed to occur before or during the sixth month of fetal brain development.
Diverse ï¬ndings appear incompatible with the theory suggesting that abnormal embryonic cell formations within the linguistic cerebral cortex have a primary role in causing dyslexia. Abnormal embryonic cell formations in dyslexics found on autopsy have also been reported in non-language cerebral and subcortical brain structures. MRI data have conï¬rmed a cerebellar role in dyslexia. Developmental dyslexia of genetic or prenatal origin has been highly correlated to a primary neurophysiological dysfunction or delayed maturation of the cerebellar and vestibular systems. Without any reasonable probability of newly and rapidly creating or dissolving primary abnormal embryonic (or other) cell formations within the brain: The acquired postnatal onset or intensiï¬cation of dyslexic reading and non-reading symptoms and related cerebellar-vestibular neurological and electronystagmographic diagnostic signs have been reported following acquired vestibular-based impairments triggered by ear and sinus infections, mononucleosis, benign paroxysmal positional vertigo, spinning and zero gravity as well as whiplash and post concussion states.
Dyslexia and its many reading and non-reading symptoms as well as their determining mechanisms have often shown rapid improvements when treated with cerebellar-vestibular stabilizing medications and related non-medical therapies. Discontinuing medication shortly after favorable therapeutic responses are obtained results in an immediate reappearance of all dyslexic symptoms and their determining mechanisms. These ï¬ndings suggest an alternative possibility that the abnormal brain cells found in dyslexic brains secondarily result from the dyslexic process and its assumed primary cerebellar-vestibular causation.
Research has examined geneâenvironment interactions in reading disability through twin studies, which estimate the proportion of variance associated with environment and the proportion associated with heritability. Studies examining the influence of environmental factors such as parental education, and teacher quality have determined that genetics have greater influence in supportive, rather than less optimal environments. Instead, it may just allow those genetic risk factors to account for more of the variance in outcome, because environmental risk factors that affect that outcome have been minimized.
As the environment plays a large role in learning and memory, it is likely that epigenetic modifications play an important role in reading ability. Animal models and measures of gene expression and methylation in the human periphery are used to study epigenetic processes, both of which have limitations in extrapolating to the human brain.