Dyslexia is characterized by difficulty with learning to readfluently and with accurate comprehension despite normalintelligence. This includes difficulty with phonological awareness, phonological decoding, processing speed,orthographic coding, auditory short-term memory, languageskills/verbal comprehension, and/or rapid naming.
Developmental reading disorder (DRD) is the most commonlearning disability. Dyslexia is the most recognized of readingdisorders, however not all reading disorders are linked todyslexia.
Adult dyslexics can read with good comprehension, althoughthey tend to read more slowly than non-dyslexics and performmore poorly at spelling and nonsense word reading, a measureof phonological awareness.
Some see dyslexia as distinct from reading difficulties resultingfrom other causes, such as a non-neurological deficiency withvision or hearing, or from poor or inadequate reading instruction. There are three proposed cognitive subtypes ofdyslexia (auditory, visual and attentional), although individualcases of dyslexia are better explained by specific underlyingneuropsychological deficits and co-occurring learningdisabilities (e.g. attention-deficit/hyperactivity disorder, mathdisability, etc.). Although it is considered to bea receptive language-based learning disability in the researchliterature, dyslexia also affects one's expressive language skills. Researchers at MIT found that people with dyslexia exhibitedimpaired voice-recognition abilities. It is believed theprevalence of dyslexia is around 5-10 percent of a givenpopulation although there have been no studies to indicate anaccurate percentage.
The World Federation of Neurology defines dyslexia as "adisorder manifested by difficulty in learning to read despiteconventional instruction, adequate intelligence and socioculturalopportunity".
The National Institute of Neurological Disorders and Strokegives the following definition for dyslexia:
Other published definitions are purely descriptive or embodycausal theories. Varying definitions are used for dyslexia fromresearchers and organizations around the world; it appears thatthis disorder encompasses a number of reading skills, deficitsand difficulties with a number of causes rather than a singlecondition.
Castles and Coltheart describe phonological and surface typesof developmental dyslexia by analogy to classical subtypes ofalexia (acquired dyslexia) which are classified according to therate of errors in reading non-words. However, thedistinction between surface and phonological dyslexia has notreplaced the old empirical terminology of dysphonetic versusdyseidetic types of dyslexia. The surface/phonologicaldistinction is only descriptive, and devoid of any etiologicalassumption as to the underlying brain mechanisms. Studieshave, however, alluded to potential differential underlying brainmechanisms in these populations given performancedifferences. The dysphonetic/dyseidetic distinctionrefers to two different mechanisms; one that relates to a speechdiscrimination deficit, and another that relates to a visualperception impairment.
However, some think that dyslexia can increase the capacity tothink and perceive multi-dimensionally and can help furtherutilize the brain’s ability to alter and create perceptions.
Signs and symptoms Edit
See also: Characteristics of dyslexia
Some early symptoms that correlate with a later diagnosis ofdyslexia include delays in speech, letter reversal or mirrorwriting, and being easily distracted by background noise. This pattern of early distractibility is partially explained by theco-occurrence of dyslexia and attention-deficit/hyperactivitydisorder. Although each disorder occurs in approximately 5% ofchildren, 25-40% of children with either dyslexia or ADHD meetcriteria for the other disorder.
At later ages symptoms can include a difficulty identifying orgenerating rhyming words, or counting syllables in words(phonological awareness), a difficulty segmenting words intoindividual sounds, or blending sounds to make words, adifficulty with word retrieval or naming problems (see anomicaphasia), commonly very poor spelling, which hasbeen called dysorthographia or dysgraphia (orthographic coding), whole-word guesses, and tendencies to omit or addletters or words when writing and reading are considered classicsigns. Other classic signs for teenagers and adults with dyslexiainclude trouble with summarizing a story, memorizing, readingaloud, and learning a foreign language.
A common misconception about dyslexia is that dyslexic readerswrite words backwards or move letters around when reading –this only occurs in a very small population of dyslexic readers.Individuals with dyslexia are better identified by readingaccuracy, fluency, and writing skills that do not seem to matchtheir level of intelligence from prior observations.
Dyslexia and biology Edit
Researchers have been trying to find a biological basis ofdyslexia since it was first identified by Oswald Berkhan in1881 and the term dyslexia coined in 1887 by Rudolf Berlin. The theories of the etiology of dyslexia have and areevolving with each new generation of dyslexia researchers, andthe more recent theories of dyslexia tend to enhance one ormore of the older theories as understanding of the nature ofdyslexia evolves (see Theories of dyslexia).
Effect of language orthography Edit
The complexity of a language's orthography (i.e. its conventionalspelling system, see orthographic depth ) has a direct impactupon how difficult it is to learn to read that language. English hasa comparatively deep orthography within the Latin alphabetwriting system, with a complex orthographic structure thatemploys spelling patterns at several levels: principally, letter-sound correspondences, syllables, and morphemes. Otherlanguages, such as Spanish, have mostly alphabeticorthographies that employ letter-sound correspondences, so-called shallow orthographies. It is relatively easy to learn toread languages like Spanish; it is much more difficult to learn toread languages with more complex orthographies such asEnglish. Logographic writing systems, notably Japanese andChinese characters, have graphemes that are not linkeddirectly to their pronunciation, which pose a different type ofdyslexic difficulty.
From a neurological perspective, different types of writingsystems (e.g. alphabetic as compared to logographic writingsystems) require different neurological pathways in order toread, write, and spell. Because different writing systems requiredifferent parts of the brain to process the visual notation ofspeech, children with reading problems in one language mightnot have a reading problem in a language with a differentorthography. The neurological skills required to perform thetasks of reading, writing, and spelling can vary between differentwriting systems. As a result, different neurological deficits cancause dyslexic problems in relation to different orthographies.
Cross-cultural prevalence Edit
Cross-cultural study of the prevalence of dyslexia is difficult asdifferent scholars and different countries often use differentcriteria to distinguish the cases of dyslexia in the continuumbetween the able and delayed readers at schools. According tothe existing literature, the prevalence of dyslexia can vary widelybetween cultures. For example, Christall reports differencesbetween 1% and 33%. According to some researchers,despite the significant differences between the writing systems,Italian, German and English populations suffer similarly fromdyslexia.
Exacerbating conditions Edit
Several learning disabilities often occur with dyslexia, but it isunclear whether these learning disabilities share underlyingneurological causes with dyslexia. These disabilities include:
- Dysgraphia – a disorder which expresses itself primarilythrough writing or typing, although in some cases it may alsoaffect eye–hand coordination, direction- or sequence-oriented processes such as tying knots or carrying out arepetitive task. In dyslexia, dysgraphia is often multifactorial,due to impaired letter writing automaticity, finger motorsequencing challenges, organizational and elaborativedifficulties, and impaired visual word form which makes itmore difficult to retrieve the visual picture of words requiredfor spelling. Dysgraphia is distinct from dyspraxia in thatdyspraxia is simply related to motor sequence impairment.
- Attention deficit disorder – a high degree of co-morbidity has been reported between ADD/ADHD anddyslexia/reading disorders, it occurs in between 12% and24% of those with dyslexia.
- Auditory processing disorder – A condition that affects theability to process auditory information. Auditory processingdisorder is a listening disability. It can lead to problemswith auditory memory and auditory sequencing. Many peoplewith dyslexia have auditory processing problems and maydevelop their own logographic cues to compensate for thistype of deficit. Auditory processing disorder is recognized asone of the major causes of dyslexia.
- Developmental dyspraxia – A neurological conditioncharacterized by a marked difficulty in carrying out routinetasks involving balance, fine-motor control, kinestheticcoordination, difficulty in the use of speech sounds, problemswith short-term memory and organization are typical ofdyspraxics.
Experience of speech acquisition delays and speech andlanguage problems can be due to problems processing anddecoding auditory input prior to reproducing their own version ofspeech, and may be observed as stuttering, cluttering orhesitant speech.
Reported findings indicate that the symptoms and related co-morbid disorders found to characterize dyslexics were consistentwith and likely determined by cerebellar-vestibulardysfunctioning mechanisms. The coexisting symptoms includeddifficulties with writing, spelling, math, memory, speech,time,concentration, distractibility, sensory input, balance,coordination,etc. All these symptoms were alsoshown to respond favorably and rapidly to cerebellar-vestibularstabilizing/enhancing medications in clinical studies.Thus these diverse symptoms and differently named disorderswere reasoned due to a common cerebellar dysfunction, ratherthan caused by differing primary cerebral processingimpairments as traditionally believed. Based on clinical andneurophysiological considerations, an alternative unifyinghypothesis was proposed. It suggested that dyslexia and all itsreading and non-reading symptoms and comorbid disordersoccurred when normal higher brain structures secondarily failedto adequately recognize and process the scrambled reading andrelated signals received; and that this signal-scrambling defectwas due to a fine- tuning impairment of primary cerebellar origin.This dyslexia hypothesis was also consistent with the presenceof validating cerebellar and vestibular neurological signs,significant compensatory and related neuroplastic capabilities, afavorable prognosis, and normal to superior mental or cerebralfunctioning and corresponding IQ's.
There is no cure for dyslexia, but dyslexic individuals can learnto read and write with educational support. There aretechniques and technical aids that can manage or even concealsymptoms of the disorder. Removing stress and anxiety alonecan improve written comprehension.
For dyslexia intervention with alphabet writing systems thefundamental aim is to increase a child's awareness ofcorrespondences between graphemes and phonemes, and torelate these to reading and spelling. It has been found thattraining focused towards visual language and orthographicissues yields longer-lasting gains than mere oral phonologicaltraining.
There is some evidence that the use of specially tailored fontsmay provide some measure of assistance for those sufferingfrom dyslexia. Intervention early on while language areasin the brain are still developing is most successful in reducinglong-term impacts of dyslexia.
Dyslexia was identified by Oswald Berkhan in 1881, but theterm dyslexia was coined in 1887 by Rudolf Berlin, who was anophthalmologist in Stuttgart. He used the term to refer to acase of a young boy who had a severe impairment in learning toread and write in spite of showing typical intellectual andphysical abilities in all other respects.
In 1896 W. Pringle Morgan, a British physician from Seaford, East Sussex, published a description of a reading-specificlearning 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 showednormal intelligence and was generally adept at other activitiestypical of children that age.
The majority of currently available dyslexia research relates tothe alphabetic writing system, and especially to languages ofEuropean origin. However, substantial research is also availableregarding dyslexia for speakers of Arabic, Chinese, and Hebrew.
In the area of neurological research into dyslexia, modernneuroimaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography(PET) have produced clear evidence of structural differences inthe brains of children with reading difficulties. It has been foundthat people with dyslexia have a deficit in parts of the lefthemisphere of the brain involved in reading, which includes theinferior frontal gyrus, inferior parietal lobule, and middle andventral temporal cortex.
Brain activation studies using PET to study language haveproduced a breakthrough in understanding of the neural basis oflanguage over the past decade. A neural basis for the visuallexicon and for auditory verbal short-term memory componentshave been proposed, with some implication that the observedneural manifestation of developmental dyslexia is task-specific(i.e., functional rather than structural).
fMRI's in dyslexics have provided important data supporting theinteractive role of the cerebellum and cerebral cortex as well asother brain structures.
Genetic research into dyslexia has its roots in the examination ofpost-autopsy brains of people with dyslexia. When theyobserved anatomical differences in the language center in adyslexic brain, they showed microscopic cortical malformationsknown as ectopias and more rarely vascular micro-malformations, and in some instances these corticalmalformations appeared as a microgyrus. These studies andthose of Cohen et al. 1989 suggested abnormal corticaldevelopment which was presumed to occur before or during thesixth month of fetal brain development.
Diverse ﬁndings appear incompatible with the theory suggestingthat abnormal embryonic cell formations within the linguisticcerebral cortex have a primary role in causing dyslexia. Abnormal embryonic cell formations in dyslexics found onautopsy have also been reported in non-language cerebral andsubcortical brain structures. MRI data have conﬁrmed acerebellar role in dyslexia. Developmental dyslexia ofgenetic or prenatal origin has been highly correlated to aprimary neurophysiological dysfunction or delayed maturation ofthe cerebellar and vestibular systems. Without anyreasonable probability of newly and rapidly creating ordissolving primary abnormal embryonic (or other) cell formationswithin the brain: The acquired postnatal onset or intensiﬁcationof dyslexic reading and non-reading symptoms and relatedcerebellar-vestibular neurological and electronystagmographicdiagnostic signs have been reported following acquiredvestibular-based impairments triggered by ear and sinusinfections, mononucleosis, benign paroxysmal positional vertigo,spinning and zero gravity as well as whiplash and postconcussion states.:5-6, 45-48, 111-112, 326, 346-349:349
Dyslexia and its many reading and non-reading symptoms aswell as their determining mechanisms have often shown rapidimprovements when treated with cerebellar-vestibular stabilizingmedications and related non-medical therapies.Discontinuing medication shortly after favorable therapeuticresponses are obtained results in an immediate reappearanceof all dyslexic symptoms and their determining mechanisms.These ﬁndings suggest an alternative possibility that theabnormal brain cells found in dyslexic brains secondarily resultfrom the dyslexic process and its assumed primary cerebellar-vestibular causation.:349
Gene-environment interaction Edit
For more details on Gene x Environment, see Gene-environment interaction.
Research has examined gene–environment interactions inreading disability through twin studies, which estimate theproportion of variance associated with environment and theproportion associated with heritability. Studies examining theinfluence of environmental factors such as parental education, and teacher quality have determined that genetics havegreater influence in supportive, rather than less optimalenvironments. Instead, it may just allow those genetic riskfactors to account for more of the variance in outcome, becauseenvironmental risk factors that affect that outcome have beenminimized.
As the environment plays a large role in learning and memory, itis likely that epigenetic modifications play an important role inreading ability. Animal models and measures of gene expression and methylation in the human periphery are used tostudy epigenetic processes, both of which have limitations inextrapolating to the human brain.
Movies about dyslexia Edit
See also Edit
- Cerebellar theory ofdyslexia
- Child development
- Deep dyslexia
- Dual-route hypothesis toreading aloud
- Dyslexie (font)
- History of the alphabet
- Learning theory (education)
- List of artistic depictions ofdyslexia
- List of people diagnosedwith dyslexia
- Philosophy of language
- Writing system
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