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Reported findings indicate that the symptoms and related co-morbid disorders found to characterize dyslexics were consistent with and likely determined by [[cerebellar]]-[[vestibular system|vestibular]] dysfunctioning mechanisms. The coexisting symptoms included difficulties with writing, spelling, math, memory, speech, time, concentration, sensory input, balance, coordination,etc.<ref name="Levinson">{{Cite book |title=A Solution to the Riddle – Dyslexia |last=Levinson |first=H.N. |year=1980 |publisher=Springer-Verlag |pages=25–71 |isbn=978-1-4613-9774-8}}</ref><ref name="Levinson2">{{Cite journal |last=Levinson |first=H. N. |year=1988 |title=The cerebellar-vestibular basis of learning disabilities in children, adolescents and adults: Hypothesis and study, perceptual motor skills |volume=67 |pages=983–1006}}</ref><ref name="Leiner">{{Cite journal|last1=Leiner |first1=H. |last2=Leiner |first2=A. |last3=Dow |first2=R. |year=1991 |title=The human cerebro-cerebellar system: Its computing, cognitive, and language skills |journal=Behavioral Brain Research |volume=44 |issue=2 |pages=113–28}}</ref><ref name="Snider">{{Cite journal|last1=Snider |first1=R.S. |last2=Stowell |first2=A. |year=1944 |title=Receiving areas of the tactile, auditory, and visual systems in the cerebellum |journal=Journal of Neurophysiology |volume=7 |pages=331–357}}</ref> All these symptoms were also shown to respond favorably and rapidly to cerebellar-vestibular stabilizing/enhancing medications in clinical studies.<ref name="Frank2">{{Cite journal|journal= Anti-motion sickness medications in dysmetric dyslexia and dyspraxia |last1=Frank |first1=J. |last2=Levinson |first2=H. N. |year=1977 |journal=Academic Therapy Publications |volume=12 |number=4 |pages=411–425}}</ref><ref name="Levinson3">{{Cite journal |last=Levinson |first=H. N. |year=1991 |title=Dramatic favorable responses of children with learning disabilities or dyslexia and attention deficit disorder to antimotion sickness medications: Four case reports |journal=Perceptual Motor Skills |volume=71 |pages=67–82}}</ref><ref name="Ayres">{{Cite journal |title=Learning disabilities and the vestibular system |journal=Journal of Learning Disabilities |last=Ayres |first=A. J. |year=1978 |volume=11 |issue=1 |pages=30–41}}</ref> Thus these diverse symptoms and differently named disorders were reasoned to be due to a common cerebellar dysfunction, rather than caused by differing primary cerebral processing impairments as traditionally believed. Based on clinical and neurophysiological considerations, an alternative unifying hypothesis was proposed. It suggested that dyslexia and all its reading and non-reading symptoms and comorbid disorders occurred when normal higher brain structures secondarily failed to adequately recognize and process the scrambled reading and related signals received; and that this signal-scrambling defect was due to a fine- tuning impairment of primary cerebellar origin. This dyslexia hypothesis was also consistent with the presence of validating cerebellar and vestibular neurological signs, significant compensatory and related neuroplastic capabilities, a favorable prognosis, and normal to superior mental or cerebral functioning and corresponding IQ's.<ref name="Solan">{{Cite journal |title=Vestibular function, sensory integration, and balance anomalies: A brief literature review |last1=Solan |first1=O. D. |first2=Harold A.|last2=Shelley-Tremblay |first3=John |last3=Larson|first4=D. |last4=Steven |year=2007 |journal=Review Optom Vis Dev |volume=38 |issue=1 |pages=1–5}}</ref><ref name="Eccles">{{Cite journal |last=Eccles |first=J.C. |title=Learning in the motor system |journal=Progress in Brain Research |year=1986 |volume=64 |pages=3–17}}</ref><ref name="Frank">{{Cite journal |last1=Frank |first1=J. |last2=Levinson |first2=H. N. |year=1976 |journal=Compensatory mechanisms in cerebellar-vestibular dysfunction, and dysmetric dyslexia and dyspraxia |journal=Academic Therapy |volume=12 |pages=5–27}}</ref>
Reported findings indicate that the symptoms and related co-morbid disorders found to characterize dyslexics were consistent with and likely determined by [[cerebellar]]-[[vestibular system|vestibular]] dysfunctioning mechanisms. The coexisting symptoms included difficulties with writing, spelling, math, memory, speech, time, concentration, sensory input, balance, coordination,etc.<ref name="Levinson">{{Cite book |title=A Solution to the Riddle – Dyslexia |last=Levinson |first=H.N. |year=1980 |publisher=Springer-Verlag |pages=25–71 |isbn=978-1-4613-9774-8}}</ref><ref name="Levinson2">{{Cite journal |last=Levinson |first=H. N. |year=1988 |title=The cerebellar-vestibular basis of learning disabilities in children, adolescents and adults: Hypothesis and study, perceptual motor skills |volume=67 |pages=983–1006}}</ref><ref name="Leiner">{{Cite journal|last1=Leiner |first1=H. |last2=Leiner |first2=A. |last3=Dow |first2=R. |year=1991 |title=The human cerebro-cerebellar system: Its computing, cognitive, and language skills |journal=Behavioral Brain Research |volume=44 |issue=2 |pages=113–28}}</ref><ref name="Snider">{{Cite journal|last1=Snider |first1=R.S. |last2=Stowell |first2=A. |year=1944 |title=Receiving areas of the tactile, auditory, and visual systems in the cerebellum |journal=Journal of Neurophysiology |volume=7 |pages=331–357}}</ref> All these symptoms were also shown to respond favorably and rapidly to cerebellar-vestibular stabilizing/enhancing medications in clinical studies.<ref name="Frank2">{{Cite journal|journal= Anti-motion sickness medications in dysmetric dyslexia and dyspraxia |last1=Frank |first1=J. |last2=Levinson |first2=H. N. |year=1977 |journal=Academic Therapy Publications |volume=12 |number=4 |pages=411–425}}</ref><ref name="Levinson3">{{Cite journal |last=Levinson |first=H. N. |year=1991 |title=Dramatic favorable responses of children with learning disabilities or dyslexia and attention deficit disorder to antimotion sickness medications: Four case reports |journal=Perceptual Motor Skills |volume=71 |pages=67–82}}</ref><ref name="Ayres">{{Cite journal |title=Learning disabilities and the vestibular system |journal=Journal of Learning Disabilities |last=Ayres |first=A. J. |year=1978 |volume=11 |issue=1 |pages=30–41}}</ref> Thus these diverse symptoms and differently named disorders were reasoned to be due to a common cerebellar dysfunction, rather than caused by differing primary cerebral processing impairments as traditionally believed. Based on clinical and neurophysiological considerations, an alternative unifying hypothesis was proposed. It suggested that dyslexia and all its reading and non-reading symptoms and comorbid disorders occurred when normal higher brain structures secondarily failed to adequately recognize and process the scrambled reading and related signals received; and that this signal-scrambling defect was due to a fine- tuning impairment of primary cerebellar origin. This dyslexia hypothesis was also consistent with the presence of validating cerebellar and vestibular neurological signs, significant compensatory and related neuroplastic capabilities, a favorable prognosis, and normal to superior mental or cerebral functioning and corresponding IQ's.<ref name="Solan">{{Cite journal |title=Vestibular function, sensory integration, and balance anomalies: A brief literature review |last1=Solan |first1=O. D. |first2=Harold A.|last2=Shelley-Tremblay |first3=John |last3=Larson|first4=D. |last4=Steven |year=2007 |journal=Review Optom Vis Dev |volume=38 |issue=1 |pages=1–5}}</ref><ref name="Eccles">{{Cite journal |last=Eccles |first=J.C. |title=Learning in the motor system |journal=Progress in Brain Research |year=1986 |volume=64 |pages=3–17}}</ref><ref name="Frank">{{Cite journal |last1=Frank |first1=J. |last2=Levinson |first2=H. N. |year=1976 |journal=Compensatory mechanisms in cerebellar-vestibular dysfunction, and dysmetric dyslexia and dyspraxia |journal=Academic Therapy |volume=12 |pages=5–27}}</ref>


do a big dump
==Management==
{{Main|Management of dyslexia|Dyslexia interventions}}
There is no cure for dyslexia, but dyslexic individuals can learn to read and write with educational support.<ref name="SwarbrickMarshall2004">{{cite book|author1=Jody Swarbrick|author2=Abigail Marshall|title=The Everything Parent's Guide To Children With Dyslexia: All You Need To Ensure Your Child's Success|url=http://books.google.com/books?id=2PdCvVMi8XMC&pg=PA93|accessdate=10 April 2012|date=10 September 2004|publisher=Everything Books|isbn=978-1-59337-135-7|pages=93–}}</ref> There are techniques and technical aids that can manage or even conceal symptoms of the disorder.<ref name="Brunswick2012">{{cite book|author=Nicola Brunswick|title=Supporting Dyslexic Adults in Higher Education and the Workplace|url=http://books.google.com/books?id=suc1o0hueowC&pg=PA115|accessdate=10 April 2012|date=10 April 2012|publisher=John Wiley & Sons|isbn=978-0-470-97479-7|pages=115–}}</ref> Removing stress and anxiety alone can improve written comprehension.<ref name="Miles2004">{{cite book|author=Thomas Richard Miles|title=Dyslexia and stress|url=http://books.google.com/books?id=h27uAAAAMAAJ|accessdate=10 April 2012|date=15 January 2004|publisher=Whurr|isbn=978-1-86156-383-5}}</ref>

For [[dyslexia intervention]] with alphabet writing systems the fundamental aim is to increase a child's awareness of correspondences between [[grapheme]]s and [[phoneme]]s, and to relate these to reading and spelling. It has been found that training focused towards visual language and [[orthography|orthographic]] issues yields longer-lasting gains than mere oral phonological training.<ref name=Lyytinen>{{Cite book
|author=Lyytinen, Heikki, Erskine, Jane, Aro, Mikko, Richardson, Ulla
|contribution=Reading and reading disorders
|editor-last=Hoff
|editor-first=Erika
|title=Blackwell Handbook of Language Development
|pages=454–474
|publisher=Blackwell
|place=
|year=2007
|isbn=978-1-4051-3253-4}}</ref>

There is some evidence that the use of specially tailored fonts may provide some measure of assistance for people who have dyslexia.<ref>{{cite web |url=http://www.scientificamerican.com/article.cfm?id=new-font-helps-dyslexics-read |title=Bold Stroke: New Font Helps Dyslexics Read |accessdate=31 October 2011 |last=Nalewicki |first=Jennifer |date=31 October 2011 |work=[[Scientific American]] |publisher=Scientific American, a Division of Nature America, Inc.}}</ref><ref>{{Cite journal |first=Renske |last=de Leeuw |title=Special Font For Dyslexia? |format=PDF |place=[[University of Twente]] |page=32 |date=December 2010 |language=English/Dutch |url=http://www.ilo.gw.utwente.nl/ilo/attachments/032_Masterthesis_Leeuw.pdf |archiveurl=http://liveweb.archive.org/http://www.ilo.gw.utwente.nl/ilo/attachments/032_Masterthesis_Leeuw.pdf |archivedate=1 November 2011 |deadurl=no}}</ref>
Intervention early on while language areas in the brain are still developing is most successful in reducing long-term impacts of dyslexia.<ref>{{cite journal |author=Chenault B, Thomson J, Abbott RD, Berninger VW |title=Effects of prior attention training on child dyslexics' response to composition instruction |journal=Developmental Neuropsychology|volume=29 |issue=1 |pages=243–60 |year=2006 |pmid=16390296 |doi=10.1207/s15326942dn2901_12 |url=http://www.tandfonline.com/doi/abs/10.1207/s15326942dn2901_12?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed}}</ref>


==History==
==History==

Revision as of 06:24, 15 October 2013

This article is about developmental dyslexia. For acquired dyslexia, see Alexia (condition).
Dyslexia
SpecialtyNeuropsychology, pediatrics Edit this on Wikidata
File:Dyslexic brain vs Normal brain.gif

Dyslexia is characterized by difficulty with learning to read fluently and with accurate comprehension despite normal intelligence.[1][2] This includes difficulty with phonological awareness, phonological decoding, processing speed, orthographic coding, auditory short-term memory, language skills/verbal comprehension, and/or rapid naming.[3][4][5]

Developmental reading disorder (DRD) is the most common learning disability. Dyslexia is the most recognized of reading disorders, however not all reading disorders are linked to dyslexia.

Some see dyslexia as distinct from reading difficulties resulting from other causes, such as a non-neurological deficiency with vision or hearing, or poor or inadequate reading instruction.[6][7] There are three proposed cognitive subtypes of dyslexia (auditory, visual and attentional), although individual cases of dyslexia are better explained by specific underlying neuropsychological deficits and co-occurring learning disabilities (e.g. attention-deficit/hyperactivity disorder, math disability, etc.).[8][9][10][11][12][13] Although it is considered to be a receptive language-based learning disability in the research literature, dyslexia also affects one's expressive language skills.[14] Researchers at MIT found that people with dyslexia exhibited impaired voice-recognition abilities.[15] It is believed the prevalence of dyslexia is around 5-10 percent of a given population although there have been no studies to indicate an accurate percentage.[8][16][17]

Classification

The World Federation of Neurology defines dyslexia as "a disorder manifested by difficulty in learning to read despite conventional instruction, adequate intelligence and sociocultural opportunity".[18]

The National Institute of Neurological Disorders and Stroke gives the following definition for dyslexia:

"Dyslexia is a brain-based type of learning disability that specifically impairs a person's ability to read. These individuals typically read at levels significantly lower than expected despite having normal intelligence. Although the disorder varies from person to person, common characteristics among people with dyslexia are difficulty with spelling, phonological processing (the manipulation of sounds), and/or rapid visual-verbal responding."[2]

Other published definitions are purely descriptive or embody causal theories. Varying definitions are used for dyslexia from researchers and organizations around the world; it appears that this disorder encompasses a number of reading skills, deficits and difficulties with a number of causes rather than a single condition.[19][20]

Castles and Coltheart describe phonological and surface types of developmental dyslexia by analogy to classical subtypes of alexia (acquired dyslexia) which are classified according to the rate of errors in reading non-words.[21][22] However, the distinction between surface and phonological dyslexia has not replaced the old empirical terminology of dysphonetic versus dyseidetic types of dyslexia.[20][22][23] The surface/phonological distinction is only descriptive, and devoid of any etiological assumption as to the underlying brain mechanisms.[24] Studies have, however, alluded to potential differential underlying brain mechanisms in these populations given performance differences.[25][26][27] The dysphonetic/dyseidetic distinction refers to two different mechanisms; one that relates to a speech discrimination deficit, and another that relates to a visual perception impairment.

However, some think that dyslexia can increase the capacity to think and perceive multi-dimensionally and can help further utilize the brain’s ability to alter and create perceptions.[28]

Signs and symptoms

See also: Characteristics of dyslexia

Some early symptoms that correlate with a later diagnosis of dyslexia include delays in speech,[29] letter reversal or mirror writing,[30][31] and being easily distracted by background noise.[32] This pattern of early distractibility is partially explained by the co-occurrence of dyslexia and attention-deficit/hyperactivity disorder. Although each disorder occurs in approximately 5% of children, 25-40% of children with either dyslexia or ADHD meet criteria for the other disorder.[33][34]

At later ages symptoms can include a difficulty identifying or generating rhyming words, or counting syllables in words (phonological awareness),[35] a difficulty segmenting words into individual sounds, or blending sounds to make words,[36] a difficulty with word retrieval or naming problems (see anomic aphasia),[37][38][39] commonly very poor spelling,[40] which has been called dysorthographia or dysgraphia (orthographic coding), whole-word guesses, and tendencies to omit or add letters or words when writing and reading are considered classic signs. Other classic signs for teenagers and adults with dyslexia include trouble with summarizing a story, memorizing, reading aloud, and learning a foreign language.[41]

A common misconception about dyslexia is that dyslexic readers write words backwards or move letters around when reading – this only occurs in a very small population of dyslexic readers.[42] Individuals with dyslexia are better identified by reading accuracy, fluency, and writing skills that do not seem to match their level of intelligence from prior observations.

In adults, dyslexia usually occurs after a brain injury or in the context of dementia. Some adults however were never identified as dyslexic when they were children or adolescents.[2] Adult dyslexics can read with good comprehension, although they tend to read more slowly than non-dyslexics and perform more poorly at spelling and nonsense word reading, a measure of phonological awareness.[43][44]

Dyslexia and biology

Researchers have been trying to find a biological basis of dyslexia since it was first identified by Oswald Berkhan in 1881[45] and the term dyslexia coined in 1887 by Rudolf Berlin.[46][47] The theories of the etiology of dyslexia have and are evolving with each new generation of dyslexia researchers, and the more recent theories of dyslexia tend to enhance one or more of the older theories as understanding of the nature of dyslexia evolves (see Theories of dyslexia).

Effect of language orthography

Main article: Orthographies and dyslexia

The complexity of a language's orthography (i.e. its conventional spelling system, see orthographic depth ) has a direct impact upon how difficult it is to learn to read that language. English has a comparatively deep orthography within the Latin alphabet writing system, with a complex orthographic structure that employs spelling patterns at several levels: principally, letter-sound correspondences, syllables, and morphemes. Other languages, such as Spanish, have mostly alphabetic orthographies that employ letter-sound correspondences, so-called shallow orthographies. It is relatively easy to learn to read languages like Spanish; it is much more difficult to learn to read languages with more complex orthographies such as English.[48] Logographic writing systems, notably Japanese and Chinese characters, have graphemes that are not linked directly to their pronunciation, which pose a different type of dyslexic difficulty.[13][49][50][51]

From a neurological perspective, different types of writing systems (e.g. alphabetic as compared to logographic writing systems) require different neurological pathways in order to read, write, and spell. Because different writing systems require different parts of the brain to process the visual notation of speech, children with reading problems in one language might not have a reading problem in a language with a different orthography. The neurological skills required to perform the tasks of reading, writing, and spelling can vary between different writing systems. As a result, different neurological deficits can cause dyslexic problems in relation to different orthographies.[49][50][51]

Cross-cultural prevalence

Cross-cultural study of the prevalence of dyslexia is difficult as different scholars and different countries often use different criteria to distinguish the cases of dyslexia in the continuum between the able and delayed readers at schools. According to the existing literature, the prevalence of dyslexia can vary widely between cultures. For example, Christall reports differences between 1% and 33%.[52] According to some researchers, despite the significant differences between the writing systems, Italian, German and English populations suffer similarly from dyslexia.[53]

Exacerbating conditions

Several learning disabilities often occur with dyslexia, but it is unclear whether these learning disabilities share underlying neurological causes with dyslexia.[54] These disabilities include:

  • Dysgraphia – a disorder which expresses itself primarily through writing or typing, although in some cases it may also affect eye–hand coordination, direction- or sequence-oriented processes such as tying knots or carrying out a repetitive task. In dyslexia, dysgraphia is often multifactorial, due to impaired letter writing automaticity, finger motor sequencing challenges, organizational and elaborative difficulties, and impaired visual word form which makes it more difficult to retrieve the visual picture of words required for spelling. Dysgraphia is distinct from developmental coordination disorder in that developmental coordination disorder is simply related to motor sequence impairment.
  • Attention deficit disorder[29][55][56] – a high degree of co-morbidity has been reported between ADD/ADHD and dyslexia/reading disorders,[57] it occurs in between 12% and 24% of those with dyslexia.[17]
  • Auditory processing disorder – A condition that affects the ability to process auditory information. Auditory processing disorder is a listening disability.[58] It can lead to problems with auditory memory and auditory sequencing. Many people with dyslexia have auditory processing problems[59] and may develop their own logographic cues to compensate for this type of deficit. Auditory processing disorder is recognized as one of the major causes of dyslexia.[60][61][62]
  • Developmental coordination disorder[29] – A neurological condition characterized by a marked difficulty in carrying out routine tasks involving balance, fine-motor control, kinesthetic coordination, difficulty in the use of speech sounds, problems with short-term memory and organization are typical of dyspraxics.

Experience of speech acquisition delays and speech and language problems can be due to problems processing and decoding auditory input prior to reproducing their own version of speech,[63][64] and may be observed as stuttering, cluttering or hesitant speech.[20]

Reported findings indicate that the symptoms and related co-morbid disorders found to characterize dyslexics were consistent with and likely determined by cerebellar-vestibular dysfunctioning mechanisms. The coexisting symptoms included difficulties with writing, spelling, math, memory, speech, time, concentration, sensory input, balance, coordination,etc.[65][66][67][68] All these symptoms were also shown to respond favorably and rapidly to cerebellar-vestibular stabilizing/enhancing medications in clinical studies.[69][70][71] Thus these diverse symptoms and differently named disorders were reasoned to be due to a common cerebellar dysfunction, rather than caused by differing primary cerebral processing impairments as traditionally believed. Based on clinical and neurophysiological considerations, an alternative unifying hypothesis was proposed. It suggested that dyslexia and all its reading and non-reading symptoms and comorbid disorders occurred when normal higher brain structures secondarily failed to adequately recognize and process the scrambled reading and related signals received; and that this signal-scrambling defect was due to a fine- tuning impairment of primary cerebellar origin. This dyslexia hypothesis was also consistent with the presence of validating cerebellar and vestibular neurological signs, significant compensatory and related neuroplastic capabilities, a favorable prognosis, and normal to superior mental or cerebral functioning and corresponding IQ's.[72][73][74]

do a big dump

History

Main article: History of developmental dyslexia

Dyslexia was identified by Oswald Berkhan in 1881,[75] but the term dyslexia was coined in 1887 by Rudolf Berlin, who was an ophthalmologist in Stuttgart.[76] 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 Percy, 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 that age.[77]

Research

Main article: Dyslexia research

The majority of currently available dyslexia research relates to the alphabetic writing system, and especially to languages of European origin. However, substantial research is also available regarding dyslexia for speakers of Arabic, Chinese, and Hebrew.[24][78][79][80][81][82]

Neuroanatomy

In the area of neurological research into dyslexia, modern neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) have produced a correlation between functional and structural differences in the brains of children and reading difficulties. Some individuals with dyslexia show less electrical activation 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.[83]

Brain activation studies using PET to study language have produced a breakthrough in 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,[84] with some implication that the observed neural manifestation of developmental dyslexia is task-specific (i.e., functional rather than structural).[85]

fMRI's in dyslexics have provided important data supporting the interactive role of the cerebellum and cerebral cortex as well as other brain structures.[86][87][88]

Genetics

Genetic research into dyslexia has its roots in the examination of post-autopsy brains of people with dyslexia.[89][90] When they observed anatomical differences in the language center in a dyslexic brain, they showed 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[91] suggested abnormal cortical development which was presumed to occur before or during the sixth month of fetal brain development.[22]

Diverse findings appear incompatible with the theory suggesting that abnormal embryonic cell formations within the linguistic cerebral cortex have a primary role in causing dyslexia.[89][92][93] Abnormal embryonic cell formations in dyslexics found on autopsy have also been reported in non-language cerebral and subcortical brain structures.[90][94] MRI data have confirmed a cerebellar role in dyslexia.[95] Developmental dyslexia of genetic or prenatal origin has been highly correlated to a primary neurophysiological dysfunction or delayed maturation of the cerebellar and vestibular systems.[66][96][97] Without any reasonable probability of newly and rapidly creating or dissolving primary abnormal embryonic (or other) cell formations within the brain: The acquired postnatal onset or intensification of dyslexic reading and non-reading symptoms and related cerebellar-vestibular neurological and electronystagmographic diagnostic signs have been reported following acquired vestibular-based impairments triggered by ear and sinus infections, mononucleosis, benign paroxysmal positional vertigo, spinning and zero gravity as well as whiplash and post concussion states.[92]: 5–6, 45–48, 111–112, 326, 346–349 [93]: 349 [98][99][100]

Dyslexia and its many reading and non-reading symptoms as well as their determining mechanisms have often shown rapid improvements when treated with cerebellar-vestibular stabilizing medications and related non-medical therapies.[69][70][72] Discontinuing medication shortly after favorable therapeutic responses are obtained results in an immediate reappearance of all dyslexic symptoms and their determining mechanisms.[70] These findings suggest an alternative possibility that the abnormal brain cells found in dyslexic brains secondarily result from the dyslexic process and its assumed primary cerebellar-vestibular causation.[93]: 349 

Gene-environment interaction

Further information: Gene-environment interaction and Gene x Environment

Research has examined gene–environment interactions in reading disability through twin studies, which estimate the proportion of variance associated with environment and the proportion associated with heritability. Studies examining the influence of environmental factors such as parental education,[101] and teacher quality[102] have determined that genetics have greater influence in supportive, rather than less optimal environments.[103] Instead, it may just allow those genetic risk factors to account for more of the variance in outcome, because environmental risk factors that affect that outcome have been minimized.[104]

As the environment plays a large role in learning and memory, it is likely that epigenetic modifications play an important role in reading ability. Animal models and measures of gene expression and methylation in the human periphery are used to study epigenetic processes, both of which have limitations in extrapolating to the human brain.[105]

Movies about dyslexia

See also

2

References

  1. ^ Yet reading difficulty is optional. (http://www.dyslexia.com/library/symptoms.htm) A child or an adult may have trouble spelling, writing, articulating, OR reading. The term dyslexia can refer to an anomalous approach to processing information. Silverman, L. (2000). The two-edged sword of compensation: How the gifted cope with learning disabilities. In Uniquely gifted: Identifying and meeting the needs of twice exceptional learners, pages 153-159.
  2. ^ a b c "Dyslexia Information Page". National Institute of Neurological Disorders and Stroke. 12 May 2010. Retrieved 5 July 2010.
  3. ^ Grigorenko, Elena L. (January 2001). "Developmental Dyslexia: An Update on Genes, Brains, and Environments". Journal of Child Psychology and Psychiatry. 42 (1): 91–125. doi:10.1111/1469-7610.00704. PMID 11205626.
  4. ^ Schulte-Körne G, Warnke A, Remschmidt H (November 2006). "[Genetics of dyslexia]". Z Kinder Jugendpsychiatr Psychother (in German). 34 (6): 435–44. doi:10.1024/1422-4917.34.6.435. PMID 17094062.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Pennington, B.F. (24 October 2011). "Individual Prediction of Dyslexia by Single Versus Multiple Deficit Models". Journal of Abnormal Psychology. 121 (1): 212–224. doi:10.1037/a0025823. PMID 22022952. {{cite journal}}: Check date values in: |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  6. ^ Stanovich KE (December 1988). "Explaining the differences between the dyslexic and the garden-variety poor reader: the phonological-core variable-difference model". Journal of Learning Disabilities. 21 (10): 590–604. doi:10.1177/002221948802101003. PMID 2465364.
  7. ^ Warnke, Andreas (19 September 1999). "Reading and spelling disorders: Clinical features and causes". Journal European Child & Adolescent Psychiatry. 8 (3): S2–S12. doi:10.1007/PL00010689. Retrieved 11 July 2010.
  8. ^ a b Czepita D, Lodygowska E (2006). "[Role of the organ of vision in the course of developmental dyslexia]". Klin Oczna (in Polish). 108 (1–3): 110–3. PMID 16883955.
  9. ^ Valdois S, Bosse ML, Tainturier MJ (November 2004). "The cognitive deficits responsible for developmental dyslexia: review of evidence for a selective visual attentional disorder". Dyslexia. 10 (4): 339–63. doi:10.1002/dys.284. PMID 15573964.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Heim S, Tschierse J, Amunts K (2008). "Cognitive subtypes of dyslexia". Acta Neurobiologiae Experimentalis. 68 (1): 73–82. ISSN 0065-1400. PMID 18389017.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ Facoetti A; Lorusso ML; Paganoni P; et al. (April 2003). "Auditory and visual automatic attention deficits in developmental dyslexia". Brain Res Cogn Brain Res. 16 (2): 185–91. doi:10.1016/S0926-6410(02)00270-7. PMID 12668226. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  12. ^ Ahissar M (November 2007). "Dyslexia and the anchoring-deficit hypothesis". Trends Cogn. Sci. (Regul. Ed.). 11 (11): 458–65. doi:10.1016/j.tics.2007.08.015. PMID 17983834.
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