As we explored yesterday, the tale of defining dyslexia began in the late 1800s when it was first known as “word blindness” and thought to be a visual processing disorder. However, overtime physicians began to untangle some of the mysteries of this unexpected difficulty with print.
Dr. James Hinshelwood, considered by many to be the father of dyslexia for his research and advocacy for clinical and social awareness of dyslexia, was the first to conclude that the cause of congenital word blindness was due to a local cerebral dysfunction rather than a generalized one (Shayowitz, 2003, p. 20). Across the Atlantic, Dr. Samuel Orton, a neurologist working with children experiencing reading difficulties in Iowa in the 1920’s, deduced that the cause was not a deficit in visual processing but rather a failure to establish hemispherical dominance (Orton, 1929) that resulted in a malfunction of the memory area of the brain rather than in the visual(Orton, 1939). Therefore, Orton played a pivotal role in defining dyslexia as a neurologically-based problem, not a visual one. Most of Orton’s suppositions, made well before brain imaging made it possible to look inside the brain, proved to be correct decades later (Geschwind, 1982).
It was the work of Norman Geschwind, a Harvard neurologist who began studying the neuroanatomy of dyslexia in the late 1960s, that began to reveal the neurophysiological makeup of the dyslexic brain. Confirming what Orton had suggested decades earlier, Geschwind found hemispherical differences in the language pathways and established that dyslexia resulted from improper fetal development (Shayowitz, 2003).
In 2001, a team of researchers lead by Eraldo Paulesu from the University of Milan conducted brain imaging studies that shed light on the neurobiological origin of dyslexia across native languages and cultures. Universally in each dyslexic—whether of Italian, French, or English background—their left temporal lobe displayed underactivation and disorganization (Dehaene, 2009).
Further brain imagining studies have revealed fascinating characteristics of the neurobiological origins of dyslexia:
- Weakness in the left occipito-temporal region, known as the “letter box” or word form area of the brain, indicates the difficulty in automatically recognizing all the letters in a word.
- Underactivation in the left temporal lobe region, such as Paulesu’s studies illuminated, indicates a core deficit in the processing the phonology of speech sounds. Difficulty with phonemic awareness undermines the acquisition of the alphabetic principal so vital to deciphering the written code.
- While the left temporal lobe shows a reduction of brain activity in dyslexics, the right temporo-parietal region is overactivated, indicating the dyslexia brain is working hard to compensate for the lack of automaticity in accessing the phonology of language.
- Another overactivated area in the dyslexic brain is Broca’s area, a region in the left inferior frontal cortex for articulation and the planning of musical movements for speech sounds. This also implies that the brain is compensating for its deficit in phonology by striving to use speech production as a bridge to decoding.
- The structure and connections of the cortex are disorganized, such as differing densities of grey matter in various parts of the cortex.
- Ectopias, incorrect placement of neurons during pregnancy, result in a “peppered” effect according to Albert Galaburda, in which some regions had too many neurons and other regions had too few. He noted that misplaced neurons tend to cluster around areas of the brain that process speech.
- Fiber bundles that connect the left temporal region to the rest of the brain are somewhat disconnected.
Clearly, the decades of brain imagining studies prove that dyslexia is a neurobiological difference that impacts, primarily, the areas of the brain that recognize letters and connect those letters to the phonology of the language. Differences in grey matter due to misplaced neurons during fetal development and impaired connections further complicate the process of acquiring literacy.
As we get closer to the 70th Annual #DyslexiaCon19 in Portland, we look forward to hearing from experts in the field of neuroscience to understand what the latest research has revealed about the origin and nature of dyslexia. We hope to see you there! Please stop by the Moose Materials booth to tell us what you learn from the conference series!
Dehaene, S. (2009). Reading in the Brain. New York: Penguin.
Geschwind, N. (1982). Why Orton Was Right. Annals of Dyslexia, 32, p13-30.
Orton, S. (1929). Sight Reading Method of Teaching Reading, As a Source of Reading Disability. Journal of Educational Psychology, 20, 135-143.
Orton, S. (1939). A Neurological Explanation of the Reading Disability. Educational Record
Shayowitz, S. (2003). Overcoming Dyslexia: A New and Complete Science-Based Program for Reading Problems at Any Level. New York: Random House.