The majority of currently available dyslexia research relates to the alphabetic writing system, and especially languages of European origin. However more research is becoming available regarding dyslexia in speakers of Hebrew and Chinese.
- Identified by Oswald Berkhan in 1881, the term 'dyslexia' was later coined in 1887 by Rudolf Berlin, an ophthalmologist practising in Stuttgart, Germany.
- In 1896, W. Pringle Morgan published a description of a reading-specific learning disorder in the British Medical Journal "Congenital Word Blindness".
- During the 1890s and early 1900s, James Hinshelwood published a series of articles in medical journals describing similar cases of congenital word blindness. In his 1917 book ''Congenital Word Blindness'', Hinshelwood asserted that the primary disability was in visual memory for words and letters, and described symptoms including letter reversals, and difficulties with spelling and reading comprehension.
- 1925 Samuel T. Orton determined that there was a syndrome unrelated to brain damage that made learning to read difficult. Orton's theory strephosymbolia described individuals with dyslexia having difficulty associating the visual forms of words with their spoken forms. Orton observed that reading deficits in dyslexia did not seem to stem from strictly visual deficits. He believed the condition was caused by the failure to establish hemispheric dominance in the brain. Orton later worked with psychologist and educator Anna Gillingham to develop an educational intervention that pioneered the use of simultaneous multisensory instruction.
- In contrast, Dearborn, Gates, Bennet and Blau considered a faulty guidance of the seeing mechanism to be the cause. They sought to discover if a conflict between spontaneous orientation of the scanning action of the eyes from right to left and training aimed at the acquisition of an opposite direction would allow an interpretation of the facts observed in the dyslexic disorder and especially of the ability to mirror-read.
- 1949 research conducted under (thesis G. Mahec Paris 1951) went further. The phenomenon is clearly linked to the dynamics of sight as it disappears when the space between letters is increased, transforming the reading into spelling. This experience also explains the ability to mirror-read.
- In the 1970s, a new hypothesis emerged: that dyslexia stems from a deficit in phonological processing or difficulty in recognizing that spoken words are formed by discrete phonemes. Affected individuals have difficulty associating these sounds with the visual letters that make up written words. Key studies suggested the importance of phonological awareness,
- 1979 Galaburda and Kemper, and Galaburda et al. 1985, reported observations from the examination of post autopsy brains of people with dyslexia. Their studies reporting observed anatomical differences in the language center in a dyslexic brain, taken with the similar work of Cohen et al. 1989, suggested abnormal cortical development, which was presumed to occur before or during the sixth month of foetal brain development.
- 1994 From post autopsy specimens Galaburda et al., reported : Abnormal auditory processing in people with dyslexia suggests that accompanying anatomical abnormalities might be present in the auditory system. Supported the reported behavioral findings of a left hemisphere-based phonological defect in dyslexic individuals.
- The development of neuroimaging technologies during the 1980s and 1990s enabled dyslexia research to make significant advances. Positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) studies have revealed the neural signature of adult normal reading (e.g. Fiez and Petersen, 1998; Turkeltaub et al., 2002) and phonological processing (e.g., Gelfand and Bookheimer, 2003; Poldrack et al., 1999). Employing various experimental approaches and paradigms (e.g., the detection or judgment of rhymes, nonword reading, and implicit reading), these studies have localized dysfunctional phonological processing in dyslexia to left-hemisphere perisylvian regions, especially for the alphabetic writing system (Paulesu et al., 2001; for review, see Eden and Zeffiro, 1998). However, it has been demonstrated that in nonalphabetic scripts, where reading places less demands on phonemic processing and the integration of visual-orthographic information is crucial, dyslexia is associated with under activity of the left middle frontal gyrus (Siok et al., 2004).
- 1999 Wydell and Butterworth reported the case study of an English-Japanese bilingual with monolingual dyslexia. Suggesting that any language where orthography-to-phonology mapping is transparent, or even opaque, or any language whose orthographic unit representing sound is coarse (i.e. at a whole character or word level) should not produce a high incidence of developmental phonological dyslexia, and that orthography can influence dyslexic symptoms
- 2003 A review by Collins and Rourke concluded that the current models of the relation between the brain and dyslexia generally focus on some form of defective or delayed brain maturation.
- 2007 Lyytinen et al. Researchers are seeking a link between the neurological and genetic findings, and the reading disorder.
- 2008 S Heim et al. in a paper "Cognitive subtypes of dyslexia" describe how they compared different sub-groups of dyslexics in comparison with a control group. This is one of the first studies not to just compare dyslexics with a non dyslexic control, but to go further and compared the different cognitive sub groups with a non dyslexic control group.
Theories of developmental dyslexia
The following theories should not be viewed as competing, but viewed as theories trying to explain the underlying causes of a similar set of symptoms from a variety of research perspectives and background.
- Cerebellar theory
One view is represented by the automaticity/cerebellar theory of dyslexia. Here the biological claim is that the cerebellum of people with dyslexia is mildly dysfunctional and that a number of cognitive difficulties ensue.
- Magnocellular theory
There is a unifying theory that attempts to integrate all the findings mentioned above. A generalization of the visual theory, the magnocellular theory postulates that the magnocellular dysfunction is not restricted to the visual pathways but is generalized to all modalities (visual and auditory as well as tactile). Slow naming speed can be identified as early as kindergarten; slow naming speed persists in adults with dyslexia.
A deficit in naming speed is hypothesized to represent a deficit that is separate from phonological processing deficit. Wolf identified four types of readers: readers with no deficits, readers with phonological processing deficit, readers with naming speed deficit, and readers with double deficit, that is, problems both with phonological processing and naming speed. Students with double deficits are most likely to have severe reading impairments.
Distinguishing among these deficits has important implications for instructional intervention. If students with double deficits receive instruction only in phonological processing, they are only receiving part of what they need.
- Perceptual visual-noise exclusion hypothesis
The concept of a perceptual noise exclusion (Impaired filtering of behaviourally irrelevant visual information in dyslexia or Visual-Noise) deficit is an emerging hypothesis, supported by research showing that subjects with dyslexia experience difficulty in performing visual tasks such as motion detection in the presence of perceptual distractions, but do not show the same impairment when the distracting factors are removed in an experimental setting. The researchers have analogized their findings concerning visual discrimination tasks to findings in other research related to auditory discrimination tasks. They assert that dyslexic symptoms arise because of an impaired ability to filter out both visual and auditory distractions, and to categorize information so as to distinguish the important sensory data from the irrelevant.
- Phonological deficit theory
The phonological deficit theory postulates that people with dyslexia have a specific impairment in the representation, storage and/or retrieval of speech sounds. It explains the reading impairment of people with dyslexia on the basis that learning to read an alphabetic system requires learning the grapheme/phoneme correspondence, i.e. the correspondence between letters and constituent sounds of speech.
- Rapid auditory processing theory
The rapid auditory processing theory is an alternative to the phonological deficit theory, which specifies that the primary deficit lies in the perception of short or rapidly varying sounds. Support for this theory arises from evidence that people with dyslexia show poor performance on a number of auditory tasks, including frequency discrimination and temporal order judgment.
That dyslexia is neurobiological in origin is supported by what Lyon et al. proclaimed as "overwhelming and converging data from functional brain imaging investigations" (2003, p. 3). The results of these studies suggest that there are observable differences in how the dyslexic brain functions when compared to the brain of a typical reader. Using fMRI, Shaywitz found that good readers show a consistent pattern of strong activation in the back of the brain with weaker activation in the front of the brain during reading tasks. In contrast, the brain activation pattern in dyslexics is the opposite during reading tasks—the frontal part of the brain becomes overactive with weaker activation in the back. Shaywitz points out "It is as if these struggling readers are using the systems in the front of the brain to try to compensate for the disruption in the back of the brain."
Brain activation studies using PET to study language have produced a breakthrough in our 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)
A University of Hong Kong study argues that dyslexia affects different structural parts of children's brains depending on the language which the children read. The study focused on comparing children that were raised reading English and children raised reading Chinese.
A University of Maastricht (Netherlands) study revealed that adult dyslexic readers underactivate superior temporal cortex for the integration of letters and speech sounds.
Molecular studies have linked several forms of dyslexia to genetic markers for dyslexia.
Several candidate genes have been identified, including at the two regions first related to dyslexia: DCDC2 and KIAA0319 on chromosome 6, and DYX1C1 on chromosome 15.
A 2007 review reported that no specific cognitive processes are known to be influenced by the proposed susceptibility genes.
A unifying theoretical framework of three working memory components provides a systems perspective for discussing past and new findings in a 12-year research program that point to heterogeneity in the genetic and brain basis and behavioral expression of dyslexia.
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