The history of dyslexia research spans from the late 1800s to the present.

Pre-1900

photograph
Adolph Kussmaul

The concept of "word-blindness" (German: "wortblindheit"), as an isolated condition, was first developed by the German physician Adolph Kussmaul in 1877.[1][2] Identified by Oswald Berkhan in 1881,[3] the term 'dyslexia' was later coined in 1887 by Rudolf Berlin,[4] an ophthalmologist practicing in Stuttgart, Germany.[5] Rudolf Berlin used the term dyslexia to describe partial reading loss in an adult patient.[2] The word is drawn from the Greek prefix δυσ- (dus-), "hard, bad, difficult"[6] + λέξις (lexis), "speech, word".[7][8] He used the term to refer to a case of a young boy who had a severe impairment in learning to read and write in spite of showing typical intellectual and physical abilities in all other respects.

In 1896, W. Pringle Morgan, a British physician, from Seaford, East Sussex published a description of a reading-specific learning disorder in a report to the British Medical Journal titled "Congenital Word Blindness". This described the case of a 14-year-old boy who had not yet learned to read, yet showed normal intelligence and was generally adept at other activities typical of children of that age. The boy could read and write all letters in the alphabet; however, had difficult in reading common monosyllabic words. The boy's spelling was extremely poor. He substituted word suffixes ("winder" for "winding") and transposed his letters within the words ("Precy" for Percy). The boy showed no difficulty in reading multidigit numbers and correctly solving problems such as (a + x)(a - x) = (a2 - x2). This led Morgan to conclude the etiology of reading disability to be congenital and attributed it to defective development of the left angular gyrus of the brain.[2]

1900-1950

During the 1890s and early 1900s, James Hinshelwood, a British ophthalmologist, published a series of articles in medical journals describing similar cases of congenital word blindness, which he defined as "a congenital defect occurring in children with otherwise normal and undamaged brains characterised by a difficulty in learning to read." 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.[9] Additionally, another British physician, CJ Thomas, provided a summary of congenital word blindness based on 100 cases at special schools in England. Thomas observed that word blindness was more prevalent than suspected. Furthermore, it appeared more than one member of the family was affected and three times more frequent in males than females. Thomas recommended that children with this disability be taught on a one-to-one bases and initially teach the alphabet be accomplished through touch by encouraging the child to handle large wooden letters.[2]

In 1925 Samuel T. Orton, a neuropsychiatrist from Iowa, who worked primarily with stroke victims, met a girl who could not read and who exhibited symptoms similar to stroke victims who had lost the ability to read. Orton began studying reading difficulties and determined that there was a syndrome unrelated to brain damage that made learning to read difficult. In 1930, Orton called his theory strephosymbolia (meaning 'twisted signs') and specific reading disability to describe individuals with dyslexia had difficulty associating the visual forms of words with their spoken forms.[10] Ironcially, others who criticized strephosymbolia because mirror writing and reversals in reading are not salient symptoms of specific reading disability. Orton used the term specific reading disability more often than strephosymbolia.[2] Orton observed that reading deficits in dyslexia did not seem to stem from strictly visual deficits.[11] He believed the condition was caused by the failure to establish hemispheric dominance in the brain.[12] He also observed that the children he worked with were disproportionately left- or mixed-handed, although this finding has been difficult to replicate.[13] Influenced by the kinesthetic work of Helen Keller and Grace Fernald, and looking for a way to teach reading using both left and right brain functions,[10] Orton later worked with psychologist and educator Anna Gillingham to develop an educational intervention that pioneered the use of simultaneous multisensory instruction.[14] Orton's 1937 book, hinged around the treatment of specific reading disabilities

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.

To this end the authors asked four adults to read a text reflected in a mirror for ten minutes a day for five months. In all subjects, the words were not perceived in their globality but required a meticulous analysis of the letters and syllables. They also demonstrated total or partial inversions even sometimes affecting the order of the words in a sentence. They revealed a curious impression of not just horizontal but also vertical inversions. These are errors that exist amongst people with dyslexia and they experience the aggravating circumstance inherent in all learning.

1950–2000

photograph
Clément Launay

In 1949, research conducted under Clement Launay (thesis G. Mahec Paris 1951) went further. In adult subjects, the reading of a series of 66 tiny lower-case letters, 5 mm high, spaced 5 mm apart, first from left to right, and then from right to left, was more easily and quickly done in the left to right direction. For former dyslexic children, a substantial number read a series of 42 letters with equal speed in both directions, and some (10%) read better from right to left than from left to right. 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 April 1963, the conference Explorations into the Problems of the Perceptually Handicapped Child, Samuel Kirk introduced the term learning disability to provide a more collective term for reading disability and other related difficulties.

In 1964, the Associated for Children with Learning Disabilities (now known as Learning Disability Association of America) was formed.[2]

In 1968, Makita suggested that dyslexia was mostly absent among Japanese children.[15] A 2005 study shows that Makita's claim of rarity of incidence of reading disabilities in Japan to be incorrect.[16]

In the 1970s, a hypothesis emerged that dyslexia stems from a deficit in phonological processing, or difficulty in recognizing that spoken words are formed by discrete phonemes, for example, that the word CAT comes from the sounds [k], [æ], and [t]. As a result, affected individuals have difficulty associating these sounds with the visual letters that make up written words. Key studies of the phonological deficit hypothesis include the finding that the strongest predictor of reading success in school age children is phonological awareness,[17] and that phonological awareness instruction can improve decoding skills for children with reading difficulties.[18]

In 1975, the passage of the Education for All Handicapped Children Act of 1975 (PL 94–142) defined learning disability as a "disorder in one or more of the basic psychological processes involved in understanding or in using spoken or written language, which may manifest itself in an imperfect ability to listen, think, speak, write, spell or to do mathematical calculations."[2]

In 1979, Galaburda and Kemper[19] and Galaburda et al. 1985,[20] reported observations from the examination of post autopsy brains of people with dyslexia. Observed anatomical differences in the language center in a dyslexic brain, showing 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,[21] suggested abnormal cortical development which was presumed to occur before or during the sixth month of foetal brain development.[22]

In 1993, Castles and Coltheart described developmental dyslexia as two prevalent and distinct varieties using the subtypes of alexia (acquired dyslexia), surface and phonological dyslexia.[23] Understanding these subtypes is useful in diagnosing learning patterns and developing approaches for overcoming visual perception impairments or speech discrimination deficits. Cestnick and Coltheart (1999) demonstrated what these underlying deficits are in part, through unveiling different profiles of phonological versus surface dyslexics.[24] Surface dyslexia is characterized by subjects who can read known words but who have trouble reading words that are irregular.[23] Phonological dyslexia is characterized by subjects who can read aloud both regular and irregular words but have difficulties with non-words and with connecting sounds to symbols, or with sounding out words. Phonological processing tasks predict reading accuracy and comprehension.[23] Cestnick and Jerger (2000)[25] and Cestnick (2001)[26] further demonstrated distinct processing differences between phonological and surface dyslexics. Manis et al. 1996, concluded that there were probably more than two subtypes of dyslexia, which would be related to multiple underlying deficits.[27]

In 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. They measured cross-sectional neuronal areas in the medial geniculate nuclei (MGNs) of five dyslexic and seven control brains. In contrast to controls, which showed no asymmetry, the left-side medial geniculate nucleus (MGN) neurons were significantly smaller than the right in the dyslexic sample. Also, as compared with controls, there were more small neurons and fewer large neurons in the left dyslexic MGN. These findings are consistent with reported behavioral findings of a left hemisphere-based phonological defect in dyslexic individuals.[28]

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., Bookheimer et al., 1995; Fiez and Petersen, 1998;[29] Price, 1997; Pugh et al., 1996; Turkeltaub et al., 2002)[30] and phonological processing (e.g., Gelfand and Bookheimer, 2003;[31] Poldrack et al., 1999;[32] Price et al., 1997; Rumsey et al., 1997a). Brain imaging studies have also characterized the anomalous patterns of neuronal activation associated with reading and phonological processing in adults with persistent or compensated developmental dyslexia (e.g., Brunswick et al., 1999;[33] Demonet et al., 1992; Flowers et al., 1991; Horwitz et al., 1998;[34] Ingvar et al., 1993; Paulesu et al., 1996; Pugh et al., 2000;[35] Rumsey et al., 1997b; Shaywitz et al., 1998).[36] 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. Differences in task-related signal change in the left temporoparietal and occipitotemporal cortices have emerged as the most consistent findings in studies of dyslexia in the alphabetic writing system (Paulesu et al., 2001;[37] for review, see Eden and Zeffiro, 1998).[38] 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).[39]

In 1999, Wydell and Butterworth reported the case study of an English-Japanese bilingual with monolingual dyslexia.[40] 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.

2000s

In 2001, Temple et al. Suggest that dyslexia may be characterized in childhood by disruptions in the neural bases of both phonological and orthographic processes important for reading.[41]

In 2002, Talcott et al. reported that both visual motion sensitivity and auditory sensitivity to frequency differences were robust predictors of children's literacy skills and their orthographic and phonological skills.[42]

In 2003, Turkeltaub et al., reported: "The complexities of pediatric brain imaging have precluded studies that trace the neural development of cognitive skills acquired during childhood. Using a task that isolates reading-related brain activity and minimizes confounding performance effects, we carried out a cross-sectional functional magnetic resonance imaging (fMRI) study using subjects whose ages ranged from 6 to 22 years. We found that learning to read is associated with two patterns of change in brain activity: increased activity in left-hemisphere middle temporal and Inferior frontal gyrus and decreased activity in right inferotemporal cortica areas. Activity in the left-posterior superior temporal sulcus of the youngest readers was associated with the maturation of their phonological processing abilities. These findings inform current reading models and provide strong support for Orton's 1925 theory of reading development."[43]

(A guide to the areas of the brain List of regions in the human brain, Cerebral hemisphere. and Cerebral cortex )

In 2003, Ziegler and colleagues argued that the dyslexia experienced by Germans and Italians was very similar to the dyslexia experienced by English speakers. This similarity of readers of different—shallow versus deep orthographic systems, supported the idea that the origin of dyslexia is mostly biological.[44]

As of 2003, current models of the relation between the brain and dyslexia generally focus on some form of defective or delayed brain maturation. More recently, genetic research has provided increasing evidence supporting a genetic origin of dyslexia.[45]

In 2004, 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.[46]

As of 2007, researchers Lyytinen et al. are searching for a link between the neurological and genetic findings, and the reading disorder. There are many previous and current theories of dyslexia, but one that has much support from research is that, whatever the biological cause, dyslexia is a matter of reduced phonological awareness, the ability to analyze and link the units of spoken and written languages.[47]

In 2008, S Heim et al. was one of the first studies not to just compare dyslexics with a non dyslexic control, but to go further and compare the different cognitive sub groups with a non dyslexic control group. Different theories conceptualise dyslexia as either a phonological, attentional, auditory, magnocellular, or automatisation deficit. Such heterogeneity suggests the existence of yet unrecognised subtypes of dyslexics with distinguishable deficits. The purpose of the study was to identify cognitive subtypes of dyslexia. Out of 642 children screened for reading ability 49 dyslexics and 48 controls were tested for phonological awareness, auditory discrimination, motion detection, visual attention, and rhythm imitation. A combined cluster and discriminant analysis approach revealed three clusters of dyslexics with different cognitive deficits. Compared to reading-unimpaired children cluster no. 1 had worse phonological awareness; cluster no. 2 had higher attentional costs; cluster no. 3 performed worse in the phonological, auditory, and magnocellular tasks. These results indicate that dyslexia may result from distinct cognitive impairments. As a consequence, prevention and remediation programmes should be specifically targeted for the individual child's deficit pattern.[48]

Also in 2008, Wai Ting Siok et al. describe how dyslexia is language dependent, and especially between alphabetic and non-alphabetic writing systems.[46]

In 2010, KK Chung et al. investigated the "Cognitive profiles of Hong Kong Chinese adolescents with dyslexia".[49]

References

  1. ↑ Beaton, Alan. Dyslexia, Reading and the Brain: A Sourcebook of Psychological and Biological Research, p. 3 (Psychology Press, 2004).
  2. 1 2 3 4 5 6 7 Aaron, PG; Joshi, R. Malatesha; Quatroche, Diana (2008). Becoming a Professional Reading Teacher. Chelsea, Michigan: Paul H. Brookes Publishing Co. pp. 222–230. ISBN 978-1-55766-829-5.
  3. ↑ Berkhan O (1917). "Uber die Wortblindheit, ein Stammeln im Sprechen und Schreiben, ein Fehl im Lesen". Neurologisches Centralblatt. 36: 914–927.
  4. ↑ Wagner, Rudolph (January 1973). "Rudolf Berlin: Originator of the term dyslexia". Annals of Dyslexia. 23 (1): 57–63. doi:10.1007/BF02653841. S2CID 144650069.
  5. ↑ "Über Dyslexie" [About dyslexia]. Archiv für Psychiatrie. 15: 276–278.
  6. ↑ δυσ-, Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus
  7. ↑ λέξις, Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus
  8. ↑ dyslexia, Online Etymology Dictionary
  9. ↑ Hinshelwood, James (1917). Congenital Word-blindness. London: H. K. Lewis & Co. Ltd. OCLC 9713889.
  10. 1 2 Orton, Samuel (1925). "Word-blindness in school children". Archives of Neurology and Psychiatry. 14 (5): 285–516. doi:10.1001/archneurpsyc.1925.02200170002001.
  11. ↑ Henry, Marcia K. (December 1998). "Structured, sequential, multisensory teaching: The Orton legacy". Annals of Dyslexia. 48 (1): 1–26. doi:10.1007/s11881-998-0002-9. S2CID 143886287.
  12. ↑ Orton, Samuel T. (7 April 1928). "Specific Reading Disability — Strephosymbolia". Journal of the American Medical Association. 90 (14): 1095–9. doi:10.1001/jama.1928.02690410007003. S2CID 72700345.
    reprinted: Orton, Samuel T. (December 1963). "Specific reading disability — Strephosymbolia". Annals of Dyslexia. 13 (1): 9–17. doi:10.1007/BF02653604. S2CID 144986711.
  13. ↑ Geschwind, N (1982). "Biological associations of left-handedness". Annals of Dyslexia. 33: 29–40. doi:10.1007/BF02647994. S2CID 143486597.
  14. ↑ Goeke, Jennifer; Kristen D. Ritchey (2006). "Orton-Gillingham and Orton-Gillingham-based reading instruction: a review of the literature". Journal of Special Education. 40 (3): 171–183. doi:10.1177/00224669060400030501. S2CID 16132344.
  15. ↑ Makita K (1968). "The rarity of reading disability in Japanese children". American Journal of Orthopsychiatry. 38 (4): 599–614. doi:10.1111/j.1939-0025.1968.tb02428.x. PMID 5661541.
  16. ↑ Hirose, Takehiko; Hatta, Takeshi (1988). "Reading disabilities in modern Japanese children". Journal of Research in Reading. 11 (2): 152–160. doi:10.1111/j.1467-9817.1988.tb00157.x.
  17. ↑ Bradley, L; Bryant, PE (1983). "Categorizing sounds and learning to read: A Causal connection". Nature. 30 (2): 419–421. Bibcode:1983Natur.301..419B. doi:10.1038/301419a0. S2CID 45647998.
  18. ↑ Alexander, A; Anderson, H; Heilman, P; Voeller, K; Torgesen, J (1991). "Phonological awareness training and the remediation of analytic decoding deficits in a group of severe dyslexics". Annals of Dyslexia. 41 (1): 193–206. doi:10.1007/BF02648086. PMID 24233765. S2CID 27022295.
  19. ↑ Galaburda, Albert M.; Thomas L. Kemper (August 1979). "Cytoarchitectonic Abnormalities in Developmental Dyslexia: A Case Study". Annals of Neurology. 6 (2): 94–100. doi:10.1002/ana.410060203. PMID 496415. S2CID 32912059.
  20. ↑ Galaburda AM, Sherman GF, Rosen GD, Aboitiz F, Geschwind N (August 1985). "Developmental dyslexia: four consecutive patients with cortical anomalies". Annals of Neurology. 18 (2): 222–33. doi:10.1002/ana.410180210. PMID 4037763. S2CID 44342859.
  21. ↑ Cohen M, Campbell R, Yaghmai F (June 1989). "Neuropathological abnormalities in developmental dysphasia". Annals of Neurology. 25 (6): 567–70. doi:10.1002/ana.410250607. PMID 2472772. S2CID 1480999.
  22. ↑ Habib M (December 2000). "The neurological basis of developmental dyslexia: an overview and working hypothesis". Brain. 123 (12): 2373–99. doi:10.1093/brain/123.12.2373. PMID 11099442.
  23. 1 2 3 Castles A, Coltheart M (May 1993). "Varieties of developmental dyslexia". Cognition. 47 (2): 149–80. doi:10.1016/0010-0277(93)90003-E. PMID 8324999. S2CID 17351782.
  24. ↑ Cestnick Laurie; Coltheart M (March 1999). "The Relationship Between Language-Processing and Visual-Processing Deficits in Developmental Dyslexia". Cognition. 71 (3): 231–55. CiteSeerX 10.1.1.56.3413. doi:10.1016/S0010-0277(99)00023-2. PMID 10476605. S2CID 18326093.
  25. ↑ Cestnick Laurie; Jerger James (October 2000). "Auditory temporal processing and lexical/nonlexical reading in developmental dyslexics". Journal of American Academy of Audiology. 11 (9): 501–513. doi:10.1055/s-0042-1748139. PMID 11057735. S2CID 15640951.
  26. ↑ Cestnick Laurie (August 2001). "Cross-modality temporal processing deficits in developmental phonological dyslexics". Brain and Cognition. 46 (3): 319–325. doi:10.1006/brcg.2000.1273. PMID 11487282. S2CID 866442.
  27. ↑ Manis FR, Seidenberg MS, Doi LM, McBride-Chang C, Petersen A (February 1996). "On the bases of two subtypes of developmental [corrected] dyslexia". Cognition. 58 (2): 157–95. doi:10.1016/0010-0277(95)00679-6. PMID 8820386. S2CID 1279963.
  28. ↑ Galaburda AM, Menard MT, Rosen GD (August 1994). "Evidence for aberrant auditory anatomy in developmental dyslexia". Proceedings of the National Academy of Sciences of the United States of America. 91 (17): 8010–3. Bibcode:1994PNAS...91.8010G. doi:10.1073/pnas.91.17.8010. PMC 44534. PMID 8058748.
  29. ↑ Fiez JA, Petersen SE (February 1998). "Neuroimaging studies of word reading". Proceedings of the National Academy of Sciences of the United States of America. 95 (3): 914–21. Bibcode:1998PNAS...95..914F. doi:10.1073/pnas.95.3.914. PMC 33816. PMID 9448259.
  30. ↑ Turkeltaub PE, Eden GF, Jones KM, Zeffiro TA (July 2002). "Meta-analysis of the functional neuroanatomy of single-word reading: method and validation". NeuroImage. 16 (3 Pt 1): 765–80. doi:10.1006/nimg.2002.1131. PMID 12169260. S2CID 8122844.
  31. ↑ Gelfand JR, Bookheimer SY (June 2003). "Dissociating neural mechanisms of temporal sequencing and processing phonemes". Neuron. 38 (5): 831–42. doi:10.1016/S0896-6273(03)00285-X. PMID 12797966. S2CID 15428976.
  32. ↑ Poldrack RA, Wagner AD, Prull MW, Desmond JE, Glover GH, Gabrieli JD (July 1999). "Functional specialization for semantic and phonological processing in the left inferior prefrontal cortex". NeuroImage. 10 (1): 15–35. CiteSeerX 10.1.1.72.4449. doi:10.1006/nimg.1999.0441. PMID 10385578. S2CID 6809429.
  33. ↑ Brunswick N, McCrory E, Price CJ, Frith CD, Frith U (October 1999). "Explicit and implicit processing of words and pseudowords by adult developmental dyslexics: A search for Wernicke's Wortschatz?". Brain. 122 (10): 1901–17. doi:10.1093/brain/122.10.1901. PMID 10506092.
  34. ↑ Horwitz B, Rumsey JM, Donohue BC (July 1998). "Functional connectivity of the angular gyrus in normal reading and dyslexia". Proceedings of the National Academy of Sciences of the United States of America. 95 (15): 8939–44. Bibcode:1998PNAS...95.8939H. doi:10.1073/pnas.95.15.8939. PMC 21181. PMID 9671783.
  35. ↑ Pugh KR, Mencl WE, Shaywitz BA, et al. (January 2000). "The angular gyrus in developmental dyslexia: task-specific differences in functional connectivity within posterior cortex". Psychological Science. 11 (1): 51–6. doi:10.1111/1467-9280.00214. PMID 11228843. S2CID 12792506.
  36. ↑ Shaywitz SE, Shaywitz BA, Pugh KR, et al. (March 1998). "Functional disruption in the organization of the brain for reading in dyslexia". Proceedings of the National Academy of Sciences of the United States of America. 95 (5): 2636–41. Bibcode:1998PNAS...95.2636S. doi:10.1073/pnas.95.5.2636. PMC 19444. PMID 9482939.
  37. ↑ Paulesu E, Démonet JF, Fazio F, et al. (March 2001). "Dyslexia: cultural diversity and biological unity". Science. 291 (5511): 2165–7. Bibcode:2001Sci...291.2165P. doi:10.1126/science.1057179. PMID 11251124. S2CID 20362533.
  38. ↑ Eden GF, Zeffiro TA (August 1998). "Neural systems affected in developmental dyslexia revealed by functional neuroimaging". Neuron. 21 (2): 279–82. doi:10.1016/S0896-6273(00)80537-1. PMID 9728909.
  39. ↑ Eden GF, Jones KM, Cappell K, et al. (October 2004). "Neural changes following remediation in adult developmental dyslexia". Neuron. 44 (3): 411–22. doi:10.1016/j.neuron.2004.10.019. PMID 15504323. S2CID 13456515.
  40. ↑ Wydell TN, Butterworth B (April 1999). "A case study of an English-Japanese bilingual with monolingual dyslexia". Cognition. 70 (3): 273–305. CiteSeerX 10.1.1.129.4911. doi:10.1016/S0010-0277(99)00016-5. PMID 10384738. S2CID 205872303.
  41. ↑ Temple E, Poldrack RA, Salidis J, et al. (February 2001). "Disrupted neural responses to phonological and orthographic processing in dyslexic children: an fMRI study". NeuroReport. 12 (2): 299–307. CiteSeerX 10.1.1.29.1083. doi:10.1097/00001756-200102120-00024. PMID 11209939. S2CID 8382716.
  42. ↑ Talcott JB, Witton C, Hebb GS, et al. (2002). "On the relationship between dynamic visual and auditory processing and literacy skills; results from a large primary-school study". Dyslexia. 8 (4): 204–25. CiteSeerX 10.1.1.513.1167. doi:10.1002/dys.224. PMID 12455851.
  43. ↑ Turkeltaub PE, Gareau L, Flowers DL, Zeffiro TA, Eden GF (July 2003). "Development of neural mechanisms for reading". Nature Neuroscience. 6 (7): 767–73. doi:10.1038/nn1065. PMID 12754516. S2CID 1256871.
  44. ↑ Ziegler JC, Perry C, Ma-Wyatt A, Ladner D, Schulte-Körne G (November 2003). "Developmental dyslexia in different languages: language-specific or universal?". J Exp Child Psychol. 86 (3): 169–93. doi:10.1016/S0022-0965(03)00139-5. PMID 14559203.
  45. ↑ Collins, David; Rourke, Byron (October 2003). "Learning-disabled Brains: A Review of the Literature". Journal of Clinical and Experimental Neuropsychology. 25 (7): 1011–1034. doi:10.1076/jcen.25.7.1011.16487. PMID 13680447. S2CID 12012395.
  46. 1 2 Siok WT, Niu Z, Jin Z, Perfetti CA, Tan LH (April 2008). "A structural–functional basis for dyslexia in the cortex of Chinese readers". Proceedings of the National Academy of Sciences of the United States of America. 105 (14): 5561–6. doi:10.1073/pnas.0801750105. PMC 2291101. PMID 18391194.
  47. ↑ Lyytinen, Heikki, Erskine, Jane, Aro, Mikko, Richardson, Ulla (2007). "Reading and reading disorders". In Hoff, Erika (ed.). Blackwell Handbook of Language Development. Blackwell. pp. 454–474. ISBN 978-1-4051-3253-4.{{cite book}}: CS1 maint: multiple names: authors list (link)
  48. ↑ Heim S, Tschierse J, Amunts K, et al. (2008). "Cognitive subtypes of dyslexia". Acta Neurobiologiae Experimentalis. 68 (1): 73–82. PMID 18389017. Archived from the original on 2018-11-04. Retrieved 2009-08-06.
  49. ↑ Chung KK, Ho CS, Chan DW, Tsang SM, Lee SH (February 2010). "Cognitive profiles of Chinese adolescents with dyslexia". Dyslexia. 16 (1): 2–23. doi:10.1002/dys.392. PMID 19544588. Archived from the original on 2010-03-05.
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.