Dyslexia; a neurological condition
The term dyslexia is made up of two parts: dys meaning not or difficult and lexia meaning words, reading or language. So quite literally, dyslexia mean difficulty with words. (Catts and Kamhi, 2005)
Dyslexia is often misunderstood with the problem of letter or word reversals (b/d, was/saw) or of letters, words, or sentences “dancing around” on the page. (Rayner, Foorman, Perfetti, Pesetsky, & Seidenberg, 2001). In fact, the reversals of words and alphabets and confusing them is common in early learning stages of life and these can not be directly diagnosed as a dyslexic problem but may lead to an underlaying reading problem.
A complete definition for dyslexia is:
Dyslexia is a specific learning disability that is neurobiological in origin. It is characterized by difficulties with accurate and/or fluent word recognition and by poor spelling and decoding abilities. These difficulties typically result from a deficit in the phonological component of language that is often unexpected in relation to other cognitive abilities and the provision of effective classroom instruction. (Lyon, Shaywitz, & Shaywitz, 2003, p. 2)
Neurobiological Aspects of Dyslexia
The most common way of investigating neurobiological origins of dyslexia is done through functional brain imaging (fMRI). Study suggests that there are differences in temporo-parieto-occipital brain regions between people with dyslexia and those who are not reading impaired. Some studies suggest differences in striate cortex (primary visual cortex V1) or extra striate cortex (encompasses multiple functional areas V3,V4,V5/MT all sensitive to motion), findings that coincide with other major researches describing anatomical lesions in posterior brain regions in acquired alexia( an acquired disorder resulting in inability to read or comprehend written language), most prominently centred on the angular gyrus.
The major connection of dyslexia in brain was found with the under activation of left hemisphere reading network consisting of Inferior Frontal Gyrus and Inferior Parietal Lobe. (Richlan et al... 2009,2011) The left IFG is a key region for language comprehension and production in human brain.
It is assumed that a reading circuit in the anterior frontal language regions exhibits activation in dyslexic readers to compensate for the dysfunction in posterior language regions. The meta-analytic findings speak for a marked distinction within left frontal regions; that is, between a left IFG region and a left precentral region, with dyslexic under activation in the former and dyslexic overactivation in the latter. The findings from the two fMRI studies (Richlan et al., 2010; Wimmer et al., 2010) provided further evidence for such a distinction. Both studies identified dyslexic under activation in the left IFG and dyslexic overactivation in left precentral/motor regions.
Heritability
Family history is one of the most important risk factors, with 23% to as much as 65% of children who have a parent with dyslexia reported to have a disorder. A rate among siblings of affected persons is of approx. 40% and among parents ranging from 27 to 49% (1) provides opportunities for early identification of affected siblings and often for delayed but helpful identification of effected adults. Linkage studies implicate loci on chromosome 6 and 15 in reading disability. (2,3)
Treatment of Dyslexia
Neurofeedback training or EEG Neurotherapy targets the symptoms of dyslexia at their foundation, the brain. Often visual, auditory, and/or executive processing deficiencies are present in those with learning disabilities, and neurofeedback directly targets these areas of brain function.
Not only can it target the primary symptoms, but also the secondary symptoms of learning disabilities including social emotional and self esteem difficulties. Neurofeedback produces long-term changes in an individual’s functioning and mental health. (SCDC Dr Shelly Hyman)
Breteler (2010) conducted research examining the improvements in children with dyslexia and specifically looked at reading and spelling.
They were able to find a significant improvement in spelling for the children that received the neurofeedback training when compared to the control group that did not receive the neurofeedback training. Also, their findings suggest that improvement in attentional processes in the brain could be partially what is contributing to the spelling improvements (Breteler, 2010). Neurofeedback resulted in a 400% improvement in reading memory, a 109% increase in reading ability, a 250% increase in reading comprehension. (4)
References:
Pennington BF, Gilger JW. How is dyslexia transmitted? In: Chase CH, Rosen GD, Sherman GF, eds. Developmental dyslexia: neural, cognitive, and genetic mechanisms. Baltimore: York Press, 1996:41-61.
Cardon, LR, Smith, SD, Fulker, DW, Kimberling, WJ, Pennington, BF, DeFries, JC. Quantitative trait locus for reading disability on chromosome 6. Science 1994;266:276-279
Grigorenko, EL, Wood, FB, Meyer, MS, et al. Susceptibility loci for distinct components of developmental dyslexia on chromosomes 6 and 15. Am J Hum Genet 1997;60:27-39
Thornton, Kirtley E., and Dennis P. Carmody. “Electroencephalogram biofeedback for reading disability and traumatic brain injury.” Child and Adolescent Psychiatric Clinics of North America 14.1 (2005): 137-162.
By Anatomography - en:Anatomography (setting page of this image), CC BY-SA 2.1
Figures and Tables by neurobiology of dyslexia by Haskins Labs
Comments