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==Overview==
==Overview==
Various methods and models have been used to study dyslexia.
Various methods and models have been used to study dyslexia.

===Genetics===
High genetic concordance found in [[twin studies]] suggest a significant genetic influence on reading ability, although the degree depends on the definition of dyslexia.<ref>{{cite journal|last=Olson|first=RK|title=Dyslexia: nature and nurture|journal=Dyslexia|year=2002|volume=8|issue=3|pages=143–159|doi=10.1002/dys.228|pmid=12222731}}</ref> [[Linkage analysis]] and [[genetic association]] studies (typically [[quantitative trait locus]] association studies, which use [[microarrays]] to look at [[single nucleotide polymorphisms]] of multiple genes at once) have been used to identify [[candidate gene]]s that may be implicated in dyslexia, which have then been confirmed in various [[Knockout mouse|knockout models]].<ref name=Guidi2018/>

As of 2018 the leading candidate genes included [[DYX1C1]] on [[chromosome 15]], [[DCDC2]] and [[KIAA0319]] on [[chromosome 6]], and [[ROBO1]] on [[chromosome 3]].<ref name=Guidi2018/><ref name="Shastry" >{{Cite journal|author=Shastry BS |title=Developmental dyslexia: an update |journal=J. Hum. Genet. |volume=52 |issue=2 |pages=104–9 |year=2007 |pmid=17111266 |doi=10.1007/s10038-006-0088-z |url=}}</ref><ref name=Bishop2009>{{cite journal|last=Bishop|first=DVM|title=Genes, cognition, and communication: insights from neurodevelopmental disorders|journal=Annals of the New York Academy of Sciences|date=March 2009|volume=1156|issue=1|pages=1–18|doi=10.1111/j.1749-6632.2009.04419.x|pmid=19338500|pmc=2805335|bibcode=2009NYASA1156....1B}}</ref><ref name=geneticlexicon>{{cite journal |vauthors=Paracchini S, Scerri T, Monaco AP |title=The genetic lexicon of dyslexia |journal=Annu Rev Genom Hum Genet |volume=8 |issue= |pages=57–79 |year=2007 |pmid=17444811 |doi=10.1146/annurev.genom.8.080706.092312 }}</ref> These genes appear to be involved in [[neuronal migration]], which has led to a theory of impaired migration during [[development of the nervous system in humans]] as a cause for developmental dyslexia.<ref name=Guidi2018>{{cite journal |last1=Guidi |first1=LG |last2=Velayos-Baeza |first2=A |last3=Martinez-Garay |first3=I |last4=Monaco |first4=AP |last5=Paracchini |first5=S |last6=Bishop |first6=DVM |last7=Molnár |first7=Z |title=The neuronal migration hypothesis of dyslexia: A critical evaluation 30 years on. |journal=The European journal of neuroscience |date=November 2018 |volume=48 |issue=10 |pages=3212-3233 |doi=10.1111/ejn.14149 |pmid=30218584}}</ref><ref>{{cite journal|last=Galaburda|first=Albert|title=Dyslexia—A molecular disorder of neuronal migration|journal=Annals of Dyslexia|year=2005|volume=55|issue=2|pages=151–165|doi=10.1007/s11881-005-0009-4|pmid=17849191}}</ref> Other genes associated with dyslexia have included [[RBFOX2]], [[ABCC13]], [[ZNF385D]], [[COL4A2]] and [[FGF18]].<ref name=Guidi2018/>

However, these genes account for a small proportion of variance in reading disability, often less than 0.5%.{{mcn|date=November 2018}} Additionally, the findings are not always replicated nor consistently supported by genome-wide association studies.<ref name=Guidi2018/> Therefore, no single gene is definitively implicated in dyslexia. A 2007 review reported that no specific cognitive processes are known to be influenced by the proposed genes and that scientists had begun to include [[neurophysiological]] (e.g., event-related potential) and imaging (e.g., functional [[MRI]]) procedures in their [[phenotype]] characterisation of people with dyslexia.<ref name=Schumacher2007/><ref name=Schumacher2007>{{cite journal|vauthors=Schumacher J, Hoffmann P, Schmäl C, Schulte-Körne G, Nöthen MM |title=Genetics of dyslexia: the evolving landscape |journal=[[Journal of Medical Genetics]] |volume=44 |issue=5 |pages=289–97 |date=May 2007 |pmid=17307837 |pmc=2597981 |doi=10.1136/jmg.2006.046516}}</ref>

It is likely that multiple genes, as well as the environment, interact to influence reading ability. The [[Generalist Genes Hypothesis]] proposes that many of the same genes are implicated within different aspects of a learning disability as well as between different learning disabilities. Indeed, there also appear to be a large genetic influence on other learning abilities, such as language skills.<ref>{{cite journal|last=Stromswold|first=Karin|title=The Heritability of Language: A Review and Metaanalysis of Twin, Adoption, and Linkage Studies.|journal=Language|date=December 2001|volume=77|issue=4|pages=647–723|doi=10.1353/lan.2001.0247}}</ref> The Generalist Genes Hypothesis supports the findings that many learning disabilities are [[comorbid]], such as [[speech sound disorder]], language impairment, and reading disability, although this is also influenced by diagnostic overlap.<ref>{{cite journal|author=Pennington BF, Bishop DVM |title= Relations Among Speech, Language, and Reading Disorders |journal=Annual Review of Psychology |year= 2009|volume=60 |pages=283–306|doi=10.1146/annurev.psych.60.110707.163548|pmid= 18652545 }}</ref>


=== Neuroimaging ===
=== Neuroimaging ===

Revision as of 03:16, 21 November 2018

Dyslexia is a neurological symptom wherein an individual experiences difficulty reading.[1] Because it first arose as a topic of research in the context of education, it is commonly referred to as a learning disability.[2] The neurological nature and underlying causes of dyslexia are an active area of research, and the distinction of dyslexia as a condition is a topic of some controversy.[3]

History

During the twentieth century, dyslexia was primarily seen as a phonological deficit (specifically phonological awareness) that resulted in a reading deficit.[4][5][6] Dyslexia was seen as an issue with reading achievement specifically, caused by deficits in discrimination of written word sounds as opposed to a broader disorder of brain function. However, much research from the 1990s onward has focused on the potential biological bases of dyslexia and understanding dyslexia as a disorder of brain function. One of the first weaknesses of the strictly phonological deficit hypothesis for dyslexia was its inability to account for the genetic link of dyslexia.[7] Specifically, it's been shown that "Relatively high heritabilities were observed for both reading ability and dyslexia indicating substantial genetic influences."[8] In a large twin study (sample 1031 twins), Gayan and Olson established that dyslexia was highly heritable, while a family study by Pennington (sample 1698 individuals) showed familial risk rates of 35-45%.[9][10]

Without a biological explanation for dyslexia, this heritability went unexplained. Not only must the heritability be explained, but also the environmental factors that protected at-risk children from developing dyslexia. Research began to focus on potential biological causes and to center the study of dyslexia in a developmental framework. A second major weakness of the strictly phonological deficit hypothesis was its strict definition of dyslexia as a reading disorder. Consequently, the various secondary symptoms were unable to be explained, including automatization deficits of both skill and knowledge acquisition, balance impairments, motor skill/writing deficits, and muscle tone underdevelopment.[6] New theories of dyslexia began to be a focus of research, with the most well established being the magnocellular deficit theory the automatization deficit theory, and the double-deficit hypothesis.[8][page needed]

Dyslexia and language orthography

Further information on Dyslexia and Language Orthography: Orthographies and dyslexia

The Orthography of language has its origins in the Writing Systems developed or adopted by each culture, which varies around the world. There are also orthological differences within each of the main writing systems.

History of developmental dyslexia

Further information: History of dyslexia research

Dyslexia was first identified by Oswald Berkhan in 1881,[11] and the term 'dyslexia' later coined in 1887 by Rudolf Berlin,[12] an ophthalmologist practicing in Stuttgart, Germany. [13] The history of dyslexia has been the history of dyslexia research.

Research and theories

Further information: Biological theories of dyslexia
Further information: Genetic research into dyslexia
Further information: Neurological research into dyslexia

The theories should not be seen 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.

The medical research of dyslexia began with the examination of post autopsy of brains from people who had dyslexia, which led to the present day genetic research regarding dyslexia. The parallel evolution of both the theories of dyslexia and the brain scan technology inspired the current interest in researching the cognitive neurological causes of dyslexia.

Overview

Various methods and models have been used to study dyslexia.

Genetics

High genetic concordance found in twin studies suggest a significant genetic influence on reading ability, although the degree depends on the definition of dyslexia.[14] Linkage analysis and genetic association studies (typically quantitative trait locus association studies, which use microarrays to look at single nucleotide polymorphisms of multiple genes at once) have been used to identify candidate genes that may be implicated in dyslexia, which have then been confirmed in various knockout models.[15]

As of 2018 the leading candidate genes included DYX1C1 on chromosome 15, DCDC2 and KIAA0319 on chromosome 6, and ROBO1 on chromosome 3.[15][16][17][18] These genes appear to be involved in neuronal migration, which has led to a theory of impaired migration during development of the nervous system in humans as a cause for developmental dyslexia.[15][19] Other genes associated with dyslexia have included RBFOX2, ABCC13, ZNF385D, COL4A2 and FGF18.[15]

However, these genes account for a small proportion of variance in reading disability, often less than 0.5%.

Additionally, the findings are not always replicated nor consistently supported by genome-wide association studies.[15] Therefore, no single gene is definitively implicated in dyslexia. A 2007 review reported that no specific cognitive processes are known to be influenced by the proposed genes and that scientists had begun to include neurophysiological (e.g., event-related potential) and imaging (e.g., functional MRI) procedures in their phenotype characterisation of people with dyslexia.[20][20]

It is likely that multiple genes, as well as the environment, interact to influence reading ability. The Generalist Genes Hypothesis proposes that many of the same genes are implicated within different aspects of a learning disability as well as between different learning disabilities. Indeed, there also appear to be a large genetic influence on other learning abilities, such as language skills.[21] The Generalist Genes Hypothesis supports the findings that many learning disabilities are comorbid, such as speech sound disorder, language impairment, and reading disability, although this is also influenced by diagnostic overlap.[22]

Neuroimaging

Magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI) are the main neuroimaging methods used to study brain structure in people with dyslexia, and functional magnetic resonance imaging (fMRI) along with EEG are used to study brain function.[23]

Visual processing

Visual processes constitute an important part of higher cortical functioning.[24] The encoding and interpretation of retinal stimulation occur at the neurological level upon reception of afferent input from the eyes. Reading, for example, requires the possession of both adequate vision and the neurological ability to process what is seen. In the past, many researchers have associated anomalies in the visual system as the main cause of dyslexia. While acknowledging that most such theories are untenable, visual system deficits have been shown to contribute to symptoms of dyslexia, such as word reversal and skipping words.[24]

A small subset of dyslexic individuals have been demonstrated to have deficits in the magnocellular visual system.[25] A compromised magnocellular system, responsible for the processing of images with high temporal frequencies and high degree of movement, might be the main contributing factor to the reported "masking" of words reported amongst dyslexic individuals.[25] Researchers posit that such a "masking" effect is due to the abnormal longevity of the visual trace produced in the magnocellular system, resulting in a lapse in acuity as effected individuals attempt to process connected text.[24]

Anomalies in saccadic movement, which are instantaneous, fast, oscillating eye movements essential for unimpaired reading have been observed in people with dyslexia. When corrected for reading ability, dyslexic individuals demonstrate below normal saccadic eye movements, suggesting that the severity reading disorders may be due to oculo-motor deficits.[26] However, further examination of the phenomenon shows that saccadic patterns in dyslexics seem to be a result and not the cause of the disorder, as decoding and comprehension failure were isolated as the antecedent for impairments in both the speed and accuracy with which dyslexics read. Also, there is no evidence that children with oculomotor impariments are at risk of developing dyslexia.[27]

Also suspected are convergence insufficiency and poor accommodation, both of which are uncommon in children, can interfere with the physical act of reading but not with decoding.[28]

Language processing

Brain activation studies using PET to study language have 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.[29] A neural basis for the visual lexicon and for auditory verbal short term memory components have been proposed. Wernicke's and Broca's areas are being recast in terms of localized components of phonological input and output. Some classical regions, such as the arcuate fasciculus, are having their "classical" roles questioned, while other regions, such as the basal temporal language zone, are growing progressively in terms of their recognized importance.[30][needs update]

Working memory

People with dyslexia have been commonly associated with working memory deficits, along with reduced activity in the pre-frontal and parietal cortex.[31]

Observed differences in the neural pattern of people with dyslexia, namely decreased activation in the left [32] and posterior [33] midfrontal gyrus (LMG, PMG) and superior parietial regions of the brain further supports the view that deficits in working memory contribute to dyslexia. LMG and PMG are commonly associated with working memory processes such as memory updating and temporal order memory.[32] Behavioral experiments in dyslexia have largely been supportive of the mediating role assumed by working memory between neurological abnormalities and dyslexic behavior.[34]

Cerebellar theory

Originally advanced by Fawcett and Nicholson in the 1990s, the cerebellar deficit hypothesis argues that biological differences in the cerebellum, most likely prenatal, cause a different development trajectory that can include motor skill deficits (including speech), automatization deficits, balance impairment, and phonological awareness. This collection of problems, in all or in any individual part, can lead to the reading deficits of dyslexia.[35]: 84 .[36][page needed]

Limitations

It is difficult to control for confounders when attempting to isolate specific causes; for example, the response to instructions by children is itself confounded by a subjects' environments, genetics and socio-economic status.[31]

Controversy

In recent years there has been significant debate on the categorization of dyslexia. In particular, Elliot and Gibbs argue that "attempts to distinguish between categories of 'dyslexia' and 'poor reader' or 'reading disabled' are scientifically unsupportable, arbitrary and thus potentially discriminatory".[37]

While acknowledging that reading disability is a valid scientific curiosity, and that "seeking greater understanding of the relationship between visual symbols and spoken language is crucial" and that while there was "potential of genetics and neuroscience for guiding assessment and educational practice at some stage in the future", they conclude that "there is a mistaken belief that current knowledge in these fields is sufficient to justify a category of dyslexia as a subset of those who encounter reading difficulties".

The Dyslexia Myth is a documentary that first aired in September 2005 as part of the Dispatches series produced by British broadcaster Channel 4.[38] Focusing only on the reading difficulties that people with dyslexia encounter the documentary says that myths and misconceptions surround dyslexia. It argues that the common understanding of dyslexia is not only false but makes it more difficult to provide the reading help that hundreds of thousands of children desperately need. Drawing on years of intensive academic research on both sides of the Atlantic, it challenged the existence of dyslexia as a separate condition, and highlighted the many different forms of reading styles.

Julian Elliot, an educational psychologist at Durham University in the United Kingdom, disputes the characterization of dyslexia as a medical condition, and believes it should be treated simply as a reading difficulty.[37] According to Elliot, "Parents don’t want their child to be considered lazy, thick or stupid. If they get called this medically diagnosed term, dyslexic, then it is a signal to all that it’s not to do with intelligence.”[39] Elliot believes that children of all levels of intelligence may struggle with learning to read, and that all can be helped by educational strategies appropriate to their needs. He feels that resources are wasted on diagnosis and testing, and favors early intervention programs for all struggling readers.[40] More recently Julian Elliot has also made reference to the 28 Definitions of Dyslexia which were documented in the Appendices of the National Research and Development Centre for Adult Literacy and Numeracy report on Developmental dyslexia in adults: a research review by Michael Rice with Greg Brooks May 2004.[41] [42]

John Everatt of the University of Surrey 2007, has suggested that:-

  • dyslexic students can be distinguished from other children with low reading achievement by testing geared to assessing their strengths as well as weaknesses
  • dyslexic children tend to score significantly better than other children, including non-impaired children, on tests of creativity, spatial memory, and spatial reasoning
  • dyslexic children also perform better than other reading-impaired children on tests of vocabulary and listening comprehension
  • dyslexic children may be better served by educational intervention which includes strategies geared to their unique strengths in addition to skill remediation

and thus recommends more comprehensive evaluation and targeted interventions.[43]

See also

References

  1. ^ https://dyslexiaida.org/dyslexia-at-a-glance/
  2. ^ http://www.dyslexia-aware.com/dawn/history-of-dyslexia
  3. ^ Elliott, Julian G; Gibbs, Simon (2008). "Does Dyslexia Exist?". Journal of Philosophy of Education. 42 (3–4): 475–491. doi:10.1111/j.1467-9752.2008.00653.x.
  4. ^ Christo, Catherine; John M. Davis; Stephen E. Brock (2009). Identifying, Assessing, and Treating Dyslexia at School. New York: Springer.
  5. ^ Ott, Philomena (2006). Teaching Children with Dyslexia: A Practical Guide. Routledge. ISBN 978-0415324540.
  6. ^ a b Reid, Gavin (2012). The Routledge Companion to Dyslexia. Taylor & Francis. ISBN 978-0415430784.
  7. ^ McGill-Franzen, Anne; Allington, Richard L. (2012). Handbook of Reading Disability Research. New York: Routledge. ISBN 978-0805853346.
  8. ^ a b Reid, Gavin, (2016). Dyslexia: A Practitioner's Handbook. Chichester : Wiley Blackwell. ISBN 978-0470760406.{{cite book}}: CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
  9. ^ Olson, RK (1999). "Reading Disability: Evidence for a Genetic Etiology". European Child & Adolescent Psychiatry. 8: 52–55.
  10. ^ Pennington BF, Gilger JW, Pauls D, Smith SA, Smith SD, DeFries JC (1991). "Evidence for Major Gene Transmission of Developmental Dyslexia". JAMA: The Journal of the American Medical Association. 266 (11): 1527–1534. doi:10.1001/jama.1991.03470110073036. PMID 1880884.
  11. ^ BERKHAN O. Neur. Zent 28 1917
  12. ^ Wagner, Rudolph (January 1973). "Rudolf Berlin: Originator of the term dyslexia". Annals of Dyslexia. 23 (1): 57–63. doi:10.1007/BF02653841. Retrieved 2009-05-12.
  13. ^ "Uber Dyslexie". Archiv für Psychiatrie. 15: 276–278.
  14. ^ Olson, RK (2002). "Dyslexia: nature and nurture". Dyslexia. 8 (3): 143–159. doi:10.1002/dys.228. PMID 12222731.
  15. ^ a b c d e Guidi, LG; Velayos-Baeza, A; Martinez-Garay, I; Monaco, AP; Paracchini, S; Bishop, DVM; Molnár, Z (November 2018). "The neuronal migration hypothesis of dyslexia: A critical evaluation 30 years on". The European journal of neuroscience. 48 (10): 3212–3233. doi:10.1111/ejn.14149. PMID 30218584. {{cite journal}}: no-break space character in |title= at position 72 (help)
  16. ^ Shastry BS (2007). "Developmental dyslexia: an update". J. Hum. Genet. 52 (2): 104–9. doi:10.1007/s10038-006-0088-z. PMID 17111266.
  17. ^ Bishop, DVM (March 2009). "Genes, cognition, and communication: insights from neurodevelopmental disorders". Annals of the New York Academy of Sciences. 1156 (1): 1–18. Bibcode:2009NYASA1156....1B. doi:10.1111/j.1749-6632.2009.04419.x. PMC 2805335. PMID 19338500.
  18. ^ Paracchini S, Scerri T, Monaco AP (2007). "The genetic lexicon of dyslexia". Annu Rev Genom Hum Genet. 8: 57–79. doi:10.1146/annurev.genom.8.080706.092312. PMID 17444811.
  19. ^ Galaburda, Albert (2005). "Dyslexia—A molecular disorder of neuronal migration". Annals of Dyslexia. 55 (2): 151–165. doi:10.1007/s11881-005-0009-4. PMID 17849191.
  20. ^ a b Schumacher J, Hoffmann P, Schmäl C, Schulte-Körne G, Nöthen MM (May 2007). "Genetics of dyslexia: the evolving landscape". Journal of Medical Genetics. 44 (5): 289–97. doi:10.1136/jmg.2006.046516. PMC 2597981. PMID 17307837.
  21. ^ Stromswold, Karin (December 2001). "The Heritability of Language: A Review and Metaanalysis of Twin, Adoption, and Linkage Studies". Language. 77 (4): 647–723. doi:10.1353/lan.2001.0247.
  22. ^ Pennington BF, Bishop DVM (2009). "Relations Among Speech, Language, and Reading Disorders". Annual Review of Psychology. 60: 283–306. doi:10.1146/annurev.psych.60.110707.163548. PMID 18652545.
  23. ^ Soriano-Ferrer, M; Piedra Martínez, E (undefined NaN). "A review of the neurobiological basis of dyslexia in the adult population". Neurologia (Barcelona, Spain). 32 (1): 50–57. doi:10.1016/j.nrl.2014.08.003. PMID 25444408. {{cite journal}}: Check date values in: |date= (help) Open access icon
  24. ^ a b c Vellutino, Frank R.; Fletcher, Jack M.; Snowling, Margaret J.; Scanlon, Donna M. (1 January 2004). "Specific reading disability (dyslexia): what have we learned in the past four decades?". Journal of Child Psychology and Psychiatry. 45 (1): 2–40. doi:10.1046/j.0021-9630.2003.00305.x. PMID 14959801.
  25. ^ a b Stein, John (1 January 2001). "The magnocellular theory of developmental dyslexia". Dyslexia. 7 (1): 12–36. doi:10.1002/dys.186. PMID 11305228.
  26. ^ Olitsky, SE; Nelson, LB (February 2003). "Reading disorders in children". Pediatric Clinics of North America. 50 (1): 213–24. doi:10.1016/s0031-3955(02)00104-9. PMID 12713114.
  27. ^ Hodgetts, DJ; Simon, JW; Sibila, TA; Scanlon, DM; Vellutino, FR (June 1998). "Normal reading despite limited eye movements". Journal of AAPOS. 2 (3): 182–3. doi:10.1016/S1091-8531(98)90011-8. PMID 10532756.
  28. ^ Granet, D. B.; Castro, E. F.; Gomi, C. F. (1 January 2006). "Reading: Do the Eyes Have It?". American Orthoptic Journal. 56 (1): 44–49. doi:10.3368/aoj.56.1.44.
  29. ^ Shaywitz, BA; Lyon, GR; Shaywitz, SE (2006). "The role of functional magnetic resonance imaging in understanding reading and dyslexia". Developmental Neuropsychology. 30 (1): 613–32. doi:10.1207/s15326942dn3001_5. PMID 16925477.
  30. ^ Chertkow, H; Murtha, S (1997). "PET activation and language". Clinical Neuroscience. 4 (2): 78–86. PMID 9059757.
  31. ^ a b Berninger, Virginia W.; Raskind, Wendy; Richards, Todd; Abbott, Robert; Stock, Pat (5 November 2008). "A Multidisciplinary Approach to Understanding Developmental Dyslexia Within Working-Memory Architecture: Genotypes, Phenotypes, Brain, and Instruction". Developmental Neuropsychology. 33 (6): 707–744. doi:10.1080/87565640802418662. PMID 19005912.
  32. ^ a b Wager, TD; Smith, EE (December 2003). "Neuroimaging studies of working memory: a meta-analysis". Cognitive, Affective & Behavioral Neuroscience. 3 (4): 255–74. doi:10.3758/cabn.3.4.255. PMID 15040547.
  33. ^ Vasic, N; Lohr, C; Steinbrink, C; Martin, C; Wolf, RC (2008-01-31). "Neural correlates of working memory performance in adolescents and young adults with dyslexia". Neuropsychologia. 46 (2): 640–8. doi:10.1016/j.neuropsychologia.2007.09.002. PMID 17950764.
  34. ^ Nicolson, RI; Fawcett, AJ; Dean, P (September 2001). "Developmental dyslexia: the cerebellar deficit hypothesis". Trends in Neurosciences. 24 (9): 508–11. doi:10.1016/S0166-2236(00)01896-8. PMID 11506881.
  35. ^ Fawcett, Angela J.; Nicolson, Roderick I. (2013). "Chapter 4:Dyslexia and the Cerebellum". In Reid, Gavin (ed.). The SAGE Handbook of Dyslexia. ISBN 9781412945134.
  36. ^ Nicolson R; Fawcett A (2010). Dyslexia, Learning, and the Brain. MIT Press. ISBN 9780262515092. {{cite book}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  37. ^ a b Elliott, Julian G.; Gibbs, Simon (2008). "Does Dyslexia Exist?". Journal of Philosophy of Education. 42 (3–4): 475–491. doi:10.1111/j.1467-9752.2008.00653.x. Retrieved 2009-06-22.
  38. ^ "The Dyslexia Myth". Dispatches. Channel 4.
  39. ^ Blair, Alexandra (2007-05-28). "Dyslexia 'is used by parents as excuse for slow children". London: Times Newspapers Ltd(United Kingdom). Retrieved 2007-05-29.
  40. ^ Moorhead, Joanna (2005-09-07). "Is dyslexia just a myth?". London: Guardian Unlimited. Retrieved 2007-05-29.
  41. ^ Rice, Michael; Brooks, Greg (2004-05-01). "Developmental dyslexia in adults: a research review". National Research and Development Centre for Adult Literacy and Numeracy. pp. *133–147. Archived from the original on 2007-10-20. Retrieved 2009-05-13. {{cite news}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  42. ^ Clark, Laura (2009-04-07). "Dyslexic children simply struggle to read': Expert claims tens of thousands are being falsely diagnosed". The Daily Mail. Associated Newspapers Ltd. Retrieved 2009-05-14.
  43. ^ Everatt, John; Weeks, Sally; Brooks, Peter (23 July 2007). "Profiles of Strengths and Weaknesses in Dyslexia and Other Learning Difficulties". Dyslexia. 14 (1): 16–41. doi:10.1002/dys.342. PMID 17659648. Retrieved 2007-07-26.

External links

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