dyslexia: Definition from Answers.com

At the end of the 19th century (1896), a case study of a boy with congenital word-blindness was reported in the British Medical Journal by W. Pringle Morgan. Percy F was described as a bright, intelligent boy, quick at games, as good as others of his age except for an inability to learn to read. In spite of laborious and persistent training, he could only spell out words of one syllable with great difficulty. This report served as a stimulus for research and debate on word-blindness. Half a century later, the term 'dyslexia' was adopted for the condition. 'Dyslexia' is derived from the Greek 'dys' (difficulty) and 'lexicos' (words). Today, developmental dyslexia is seen as a complex neurological condition occurring in about 4 per cent of the population and is a legally recognized disability.

The criteria for recognizing the existence of a condition are that it should have a distinct aetiology, identifying characteristics, and a prognosis, and should respond to intervention. There has been a lot of controversy about the extent to which dyslexia meets these requirements and in the UK the term 'specific learning difficulties' was preferred for use in legislation ('specific learning disabilities' in the USA). The word 'dyslexia', however, has continued to be used in cognitive research and has entered everyday parlance to such an extent that the legal term in the UK has been changed to 'specific learning difficulties (for example, dyslexia)'. The definition of dyslexia and its subtypes, and programmes for remediation, continue to evolve with developments in research and understanding of the condition.

In the 1980s and 1990s, the dominant theoretical framework for dyslexia research focused on phonological deficits. These include difficulty segmenting words into phonemes, in keeping strings of sounds or letters in short-term memory, in repeating long non-words and in reading and writing short ones, and slowness in naming colours, numbers, letters, or objects in pictures. The association between poor phonological awareness and later reading difficulty has been demonstrated across different languages, ages, and tasks. The emphasis on phonological difficulty is seen in the Orton Society (now the International Dyslexia Association) Research Committee's definition of 1994. In this, dyslexia is seen as a specific language-based disorder of constitutional origin characterized by difficulties in single word coding, usually reflecting insufficient phonological processing abilities. Such difficulties are unexpected in relation to age and other cognitive and academic abilities and are not the result of generalized developmental disability or sensory impairment. Dyslexia is seen not only as a problem with learning to read but also in acquiring proficiency in writing and spelling.

Much remedial help for dyslexic children has focused largely on the provision of multisensory phonic programmes involving the systematic teaching of letter–sound correspondences. Many dyslexic children learn to read fairly accurately but they read slowly. The positive effects of phonological support are largely on reading accuracy with relatively little effect on reading fluency. Research on speed of processing has shown a strong relationship between early letter-naming speed and later reading fluency. A 'double deficit' hypothesis for dyslexia led to the suggestion that effective remedial programmes should contain not only phonologically based instruction but also a systematic and comprehensive support directed at developing reading fluency and comprehension.

Over the last two decades, there has been a growing interest in visual processing problems in relation to text. In 1980, Olive Meares, a teacher in New Zealand, described the difficulties reported by some children of dealing with glare from the printed page when reading. At about the same time, Helen Irlen, in California, was exploring the use of tinted lenses to alleviate a problem which she called scotopic sensitivity syndrome. Irlen centres were set up in several countries to supply tinted lenses using her techniques. This triggered a great deal of interest in visual processing difficulties and poor reading, particularly as only some dyslexic children appear to benefit from using coloured overlays or tinted lenses.

In the early 1970s, Arnold Wilkins was interested in the 4 per cent of people with epilepsy who experience visually induced seizures. He noted that susceptibility to visual discomfort is most pronounced in people who suffer from frequent severe headaches. He went on to argue that reading can provoke 'pattern glare' which can result in eyestrain and headaches, and even visual illusions and seizures. Electric lighting changes in brightness twice during each cycle of the alternating electricity supply and fluorescent lighting pulsates even faster. Wilkins suggested that, although the pulsations from such lights are too fast to be seen as flicker, they affect the firing of the visual neurons in the eye. In 1991, he examined twenty volunteers with a history of reading difficulty who had been selected by the Irlen Centre in London as having benefited from the use of tinted glasses. Seventeen of them had a history of migraine in the family; nearly all of them reported a reduction in headaches when wearing their tinted glasses. To investigate this finding systematically, he built a colorimeter for the intuitive manipulation of colour (hue) and depth of colour (saturation), and developed a Rate of Reading Test to identify the poor readers who would benefit from using coloured overlays on the printed page. There is now good research evidence that some poor readers, particularly those with a family history of migraine, can be helped in this way, and that this is due neither to a placebo nor a Hawthorne effect (Wilkins 1995).

Poor readers sometimes display erratic eye movements which appear to be associated with blurring of print, letters jumping over other letters, and letter reversals. Stein and Fowler (1985) reported a study on the effect of monocular occlusion on reading in dyslexic children. They suggested that the experience of an unstable visual world when reading could be attributed to unstable vergence control of the eyes and that this could be improved by the occlusion of one eye. This was open to the objection, however, that a relationship between vergence control and the experiences reported had not been shown to be causal. In 2000, they attempted to set up a double-blind randomized controlled trial to test this. One hundred and forty-three children were selected as dyslexic with unstable binocular control from a sample of 300 7-to 11-years-olds who had been referred to a learning disabilities clinic. The children were randomly assigned to wear spectacles with pale yellow lenses with or without the left eye occluded for all reading and writing activities for nine months. They were tested without their spectacles every three months by researchers who did not know whether they belonged to the occluded or non-occluded group. At the end of nine months, there was no difference in the number of children who achieved stable binocular control but the occluded group achieved it earlier and had gained an advantage in reading performance which was maintained throughout the study. It was of course impossible for the children, parents, or teachers to be unaware of whether a child was in the occluded or non-occluded group.

Evidence has accumulated about differences in the symmetry of the cerebral hemispheres in dyslexics and controls and on the predominant location of language processing in the left hemisphere. Much detailed research has been done on the visual system and its responses to different types of visual stimuli.

In 1980, Bill Lovegrove and his colleagues suggested that dyslexic readers have low-level impairments of the transient visual system. The transient (magnocellular) visual system carries fast low-contrast information and is responsible for detecting moving stimuli but does so with poor acuity. The sustained (parvocellular) system transmits information more slowly but with high acuity. In 1991, Margaret Livingstone and her co-workers examined the functioning of the magnocellular and parvocellular divisions of the visual system by recording visually evoked potentials in response to high-and low-contrast stimuli in dyslexic and non-dyslexic people. There were no differences between the groups for the high-contrast stimuli but there were for the low. With Albert Galaburda, she and their co-workers went on to carry out a series of histological postmortem studies of the brains of people known to have been dyslexic and to compare them with non-dyslexic controls. They found that whilst the magnocellular and parvocellular layers of the lateral geniculate nucleus were clearly separated in the controls they were more merged together in the brains of the dyslexics. Moreover, the magnocellular neurons in the dyslexics were about 30 per cent smaller than in the controls. Both the magnocellular and parvocellular layers receive neuronal projections from the ganglion cells of the retina at the back of the eye. Ninety per cent of these are parvocells which signal fine detail and colour and the remainder are larger magnocells which signal the timing of visual events. Differences have since been found between dyslexics and controls in the magnocells of the auditory thalamic relay associated with the processing of sounds.

The critical factor behind fluent word reading appears to be the ability to recognize letters, spelling patterns, and whole words effortlessly and automatically. Rod Nicolson and Angela Fawcett (1990) explored the idea of automaticity suggesting that dyslexic children have difficulties in making some cognitive and motor skills automatic in spite of intensive practice. A conscious compensation hypothesis was invoked to explain why in spite of more limited automaticity many dyslexic children are able to perform at apparently normal levels in most areas, most of the time. There is growing evidence that there are differences between dyslexics and controls in motor coordination and balance. Motor skills training can improve performance on motor tasks and it was suggested in the early 1970s that motor skills intervention could help learning-disabled children. A longitudinal evaluation of a balance remediation exercise training programme for dyslexic children and matched controls is currently under way in the UK.

It has been shown recently, using positron emission tomography (PET), that in comparison with controls, dyslexics showed less activation of the cerebellum during a motor learning task. In addition, the metabolism of the cerebellum has been shown to be lower in dyslexics than controls. Research using magnetic resonance imaging (MRI) in the USA has provided evidence of the involvement and integration of seventeen regions in the brain, including the cerebellum, in reading. The cerebellum contains and receives considerable inputs from the magnocells and recent histological study of the cerebellum has confirmed cerebellar differences between dyslexics and controls.

John Stein, Joel Talcott, and Caroline Whitton (2001) suggested that the influence of polyunsaturated fatty acids (PUFAs) on the magnocell membrane may be under the control of a particular enzyme that is higher in dyslexics than controls. They think that the decline of eating fish in modern diets has led to lower levels of PUFAs. Research is under way on supplementing the diets of dyslexic children with particular omega-3 fatty acids found in some fish oils and on a breath test to identify children who may benefit from this. They also suggested that individual differences in magnocellular sensitivity may be under genetic control.

Familial clustering of dyslexia is well documented. Strong support for genetic influences rather than a shared family environment comes from studies which have found twice the rate of dyslexia in monozygotic twins who have almost identical genetic make-up, compared with dizygotic twins who have about half their genes in common. Techniques in molecular genetics have so far identified loci on chromosomes 2, 4, 6, 13, and 18 as being implicated in dyslexia. Several authors have pointed out that some of these genetic markers occur in the same regions as genes involved in some autoimmune diseases which have an increased prevalence in dyslexics. Although considerable advances have been made, understanding the biological basis of dyslexia is still at a relatively early stage, and significant questions remain about its genetic basis and the brain mechanisms involved.

Since the identification of pre-reading correlates of dyslexia, considerable efforts have been made to develop early screening programmes; this is difficult because early childhood development is so variable but a recent study compared the literacy skills of children at genetic risk of dyslexia with those with no such family history. The children at genetic risk were more likely to have slower speech and language development at 4 years of age and literacy problems at age 6. It appears that early childhood screening should be sequential to allow for differences in rates of development and treated as probabilistic. Developments in screening and assessing the difficulties of school children and adults now include work on computerized screening and assessment.

In describing the pattern of difficulties in dyslexia, Tim Miles (1993) pointed out that dyslexia involves more than a language and literacy problem. Certainly there can be considerable individual differences in schoolchildren and adults with dyslexia, not least because many develop individual coping and compensatory strategies. For some, the extent to which their dyslexic difficulties will impair performance at work will be minimal but for others it may result in working in occupations which do not make full use of their real abilities and potential. The stress of coping with dyslexia at school, college or university, and work is well documented (e.g. Miles and Varma 1995). Information on screening, assessment, intervention, and current legislation affecting children and adults is available on the websites of the British Dyslexia Association, the Dyslexia Institute, and the International Dyslexia Association.

(Published 2004)

— Mary N. Haslum

Bibliography

Bradley, L., and Bryant, P. (1983). 'Categorizing sounds and learning to read'. Nature.
Livingstone, M. S., Rosen, G. D., Drislane, F. W., and Galaburda, A. M. (1991). 'Physiological and anatomical evidence for a magnocellular defect in developmental dyslexia'. Proceedings of the National Academy of Sciences of the USA, 88.
Lovegrove, W. J., Martin, F., Blackwood, M., and Badock, D. (1980). 'Specific reading difficulty: differences in contrast sensitivity as a function of spatial frequency'. Science, 210.
Miles, T. R. (1993). Dyslexia: The Pattern of Difficulties (2nd edn.).
— — and Varma, V. (1995). Dyslexia and Stress.
Morgan, W. P. (1896). 'A case study of congenital word blindness'. British Medical Journal, 2.
Nicolson, R. I., and Fawcett, A. J. (1990). 'Automaticity: a new framework for dyslexia research'. Cognition, 35/2.
Orton Society Research Committee (1994). 'Dyslexia'. Perspectives, 20.
Stein, J. F., and Fowler, S. (1985). 'Effect of monocular occlusion on reading in dyslexic children'. Lancet, 13 July.
— — Talcott, J., and Whitton, C. (2001). 'The senorimotor basis of developmental dyslexia'. In Fawcett, A. J. (ed.), Dyslexia Theory and Good Practice.
Wilkins, A. (1995). Visual Stress.
Websites:www.bda-dyslexia.org.uk
www.dyslexia-inst.org.uk
www.interdys.org

This article is about developmental dyslexia. For acquired dyslexia, see Alexia (acquired dyslexia).

Dyslexia
Classification and external resources
ICD-10	R 48.0
ICD-9	315.02
OMIM	127700
DiseasesDB	4016
MeSH	D004410

Dyslexia is a very broad term defining a learning disability that impairs a person's fluency or comprehension accuracy in being able to read,^[1] and which can manifest itself as a difficulty with phonological awareness, phonological decoding, orthographic coding, auditory short-term memory, or rapid naming.^[2]^[3] Dyslexia is separate and distinct from reading difficulties resulting from other causes, such as a non-neurological deficiency with vision or hearing, or from poor or inadequate reading instruction.^[4]^[5] It is believed that dyslexia can affect between 5 and 10 percent of a given population although there have been no studies to indicate an accurate percentage.^[6]^[7]^[8]

There are three proposed cognitive subtypes of dyslexia: auditory, visual and attentional.^[7]^[9]^[10]^[11]^[12]^[13] Reading disabilities, or dyslexia, is the most common learning disability, although in research literature it is considered to be a receptive language-based learning disability.^[14] Researchers at MIT found that people with dyslexia exhibited impaired voice-recognition abilities.^[15]

Accomplished adult dyslexics may be able to read with good comprehension, but they tend to read more slowly than non-dyslexics and may perform more poorly at nonsense word reading (a measure of phonological awareness) and spelling.^[16] Dyslexia is not an intellectual disability, since dyslexia and IQ are not interrelated, as a result of cognition developing independently.^[17]

Classification

Spoken language is a universal form of human communication. The visual notation of written language is not found in all cultures and is relatively new with regards to human evolution.^[18]

There are many definitions of dyslexia but no official consensus has been reached.

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".^[19]

MedlinePlus and the National Institutes of Health define dyslexia as "a reading disability resulting from the inability to process graphic symbols".^[20]

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. In adults, dyslexia usually occurs after a brain injury or in the context of dementia. It can also be inherited in some families and so on, and recent studies have identified a number of genes that may predispose an individual to developing dyslexia".^[1]

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.^[21]^[22]

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.^[23]^[24] However, the distinction between surface and phonological dyslexia has not replaced the old empirical terminology of dysphonetic versus dyseidetic types of dyslexia.^[22]^[24]^[25] The surface/phonological distinction is only descriptive, and devoid of any aetiological assumption as to the underlying brain mechanisms (Galaburda and Cestnick 2003).^[26] Studies have, however, alluded to potential differential underlying brain mechanisms in these populations given performance differences (Cestnick et al.).^[27]^[28]^[29] 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.

Signs and symptoms

Common Symptoms

The symptoms of dyslexia vary according to the severity of the disorder as well as the age of the individual. Some common ones are:

Appears bright, highly intelligent, and articulate, but unable to read, write, or spell at grade level
Labeled lazy, dumb, careless, immature, "not trying hard enough," or "behavior problem"
Isn't "behind enough" to be helped in the school setting
High in IQ, yet may not test well academically
Tests well orally, but not written
Feels dumb and has poor self esteem
Easily frustrated and emotional about school, reading, or testing
Talented in art, drama, music, sports, mechanics, story- telling, sales, business, designing, building, and/or engineering.
Seems to zone out or daydream.
Difficult to sustain attention; seems hyper.
Learns best through "hands-on" experience.
Complains of dizziness, headaches, or stomach aches while reading.
Confused by letters, numbers, words, sequences, and/or verbal explanations
Reading or writing shows repetitions, additions, transpositions, omissions, substitutions, and reversals in letters, numbers, and/or words.
Complains of feeling or seeing non-existent movement while reading, writing, or copying words and letters.
Seems to have difficulty with vision, but eye exams and tests don't seem to reveal a problem.
Keen sighted and observant, or lacks depth perception and peripheral vision.
Reads and rereads with little comprehension.
Spells phonetically and inconsistently.
Has extended hearing; hears things that most people can't hear.
Easily distracted by sounds.
Difficulty putting thoughts into words, speaks in halting phrases
Leaves sentences incomplete
Stutters under stress
Mispronounces long words
Transposes phrases, words, and syllables when speaking.
Trouble with writing or copying
Pencil grip is unusual
Handwriting varies or is illegible.
Clumsy, uncoordinated, and is not very good at ball or team sports.
Difficulty with fine and/or gross motor skills and tasks
Prone to motion sickness
Can be ambidextrous, and often confuses left and right, and over and under.
Has difficulty telling time, bad at time management, learning sequences information or tasks
Has difficulty being on time.
Computing math shows dependance on finger counting and other tricks
Knows answers, but can't do it on paper.
Can count, but bad at counting objects and dealing with money.
Can do arithmetic and math, but fails word problems
Cannot grasp algebra or higher math.
Excellent long- term memory for experiences, locations, and faces.
Poor memory for sequences, facts, and information that has not been experienced.
Thinks primarily with images and feeling, not sounds or words.
Little internal dialogue.
Extremely disorderly or compulsively orderly
Can be class clown, trouble maker, or too quiet.
Unusually early or late developmental stages.
Prone to ear infections
Sensitive to foods, additives, and chemical products.
Can be an extra deep or light sleeper
Bed-wetting beyond appropriate age.
Unusually high or low tolerance for pain.
Strong sense of justice
Emotionally sensitive
Strives for perfection
Mistakes and symptoms increase dramatically with confusion, time pressure, emotional stress, or poor health.
Massive willy

Preschool-aged children

It is difficult to obtain a certain diagnosis of dyslexia before a child begins school, but many dyslexic individuals have a history of difficulties that began well before kindergarten. Children who exhibit these symptoms early in life have a higher likelihood of being diagnosed as dyslexic than other children. These symptoms include:

delays in speech^[30]
slow learning of new words
difficulty in rhyming words, as in nursery rhymes
low letter knowledge
letter reversal or mirror writing^[31]^[32] (for example, "Я" instead of "R")
easily distracted by background noise^[33]

Early primary school children

Difficulty learning the alphabet or letter order
Difficulty with associating sounds with the letters that represent them (sound-symbol correspondence)
Difficulty identifying or generating rhyming words, or counting syllables in words^[34] (phonological awareness)
Difficulty segmenting words into individual sounds, or blending sounds to make words^[35] (phonemic awareness)
Difficulty with word retrieval or naming problems^[36]^[37]^[38]
Difficulty learning to decode written words
Difficulty distinguishing between similar sounds in words; mixing up sounds in polysyllabic words (auditory discrimination) (for example, "aminal" for animal, "bisghetti" for spaghetti)
Often have reduced memory, executive function, and goal directed behavior^[39]

Older primary school children

Slow or inaccurate reading
Very poor spelling^[40] which has been called dysorthographia (orthographic coding)
Difficulty reading out loud, reading words in the wrong order, skipping words and sometimes saying a word similar to another word (auditory processing disorder)
Difficulty associating individual words with their correct meanings
Difficulty with time keeping and concept of time when doing a certain task
Difficulty with organization skills (working memory)
Children with dyslexia may fail to see (and occasionally to hear) similarities and differences in letters and words, may not recognize the spacing that organizes letters into separate words, and may be unable to sound out the pronunciation of an unfamiliar word (auditory processing disorder)
Tendencies to omit or add letters or words when writing and reading^[41]

Secondary school children and adults

Some people with dyslexia are able to disguise their weaknesses, even from themselves. Many students reach higher education before they encounter the threshold at which they are no longer able to compensate for their learning weaknesses.

One common misconception about dyslexia is that dyslexic readers write words backwards or move letters around when reading. In fact, this only occurs in a very small population of dyslexic readers. Dyslexic people are better identified by writing that does not seem to match their level of intelligence from prior observations. Additionally, dyslexic people often substitute similar-looking, but unrelated, words in place of the ones intended (what/want, say/saw, help/held, run/fun, fell/fall, to/too, who/how etc.)^{[citation needed]}.

Comorbidities

Several learning disabilities often occur with dyslexia, but it is unclear whether these learning disabilities share underlying neurological causes with dyslexia.^[42] These disabilities include, but are not limited to:

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 dyspraxia in that dyspraxia is simply related motor sequence impairment.
Dyscalculia— a neurological condition characterized by a problem with basic sense of number and quantity and difficult retrieving rote math facts. Often people with this condition can understand very complex mathematical concepts and principles but have difficulty retrieving basic math facts involving addition and subtraction.
Attention Deficit Disorder — a high degree of co-morbidity has been reported between ADD / ADHD and dyslexia/reading disorders,^[43] although the contributions of dyslexia-related challenges such as auditory verbal working memory to attention issues has not been well established

Cause

Main article: Theories of dyslexia

Since the symptoms of dyslexia were first identified by Oswald Berkhan in 1881,^[44] and the term 'dyslexia' coined in 1887 by Rudolf Berlin,^[45]^[46] generations of researchers have been investigating what dyslexia is and trying to identify the biological causes. 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. Theories should not be viewed as competing, but as attempting to explain the underlying causes of a similar set of symptoms from a variety of research perspectives and background.^[47]^[48]

Effect of language orthography

Main article: Orthographies and dyslexia

The complexity of a language's orthography or spelling system – formally, its orthographic depth – has a direct impact on 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 alphabetic orthographies that employ only 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.^[49] 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]^[50]^[51]^[52]

From a neurological perspective, different types of writing system, for example 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 and as a result different neurological deficits can cause dyslexic problems in relation to different orthographies.^[50]^[51]^[52]

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%.^[53] Some populations (for example, Japanese and Chinese) may have relatively small number of dyslexic schoolchildren,^[54] and some populations (for example, European, and particularly sub-Saharan African populations) might have higher dyslexia prevalence. According to some researchers, despite the significant differences between the writing systems, Italian, German and English populations suffer similarly from dyslexia.^[55]

Exacerbating conditions

Dyslexia is attributed to neurological factors that influence the individual's ability to read, write, and spell written language.^[24]

The following conditions may be contributory or overlapping factors, as they can lead to difficulty in reading:

Aphasia - neurologically based speech disorders, which can cause alexia (acquired dyslexia).
Attention deficit hyperactivity disorder -^[30]^[56]^[57] A disorder that occurs in between 12% and 24% of those with dyslexia.^[8]
Auditory processing disorder - A condition that affects the ability to process auditory information. Auditory processing disorder is a listening disability.^[58]^{[unreliable source?]} It can lead to problems with auditory memory and auditory sequencing. Many people with dyslexia have auditory processing problems including history of auditory reversals,^{[citation needed]} 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.^[58]^[59]^[60]^[61] Some children can acquire auditory processing disorder as a result of experiencing otitis media with effusion (glue ear, sticky ear, grommets) and other severe ear conditions.^[62]
Developmental dyspraxia -^[30] 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.
Scotopic sensitivity syndrome, also known as Irlen Syndrome - A term used to describe sensitivity to certain wavelengths of light which interfere with visual processing.^[63]^[64]
Specific language impairment (SLI) - A developmental language disorder that can affect both expressive and receptive language. SLI is defined as a "pure" language impairment, meaning that is not related to or caused by other developmental disorders, hearing loss or acquired brain injury. A study by the Universities of Maastricht and Utrecht examined speech perception and speech production in 3-year-old Dutch children at familial risk of developing dyslexia. Their performance in speech sound categorization and their production of words was compared to that of age-matched children with SLI and typically developing controls. The results of the at-risk and SLI-group were highly similar. Analysis of the individual data revealed that both groups contained subgroups with good and poorly performing children. Their impaired expressive phonology seemed to be related to a deficit in speech perception. The findings indicate that both dyslexia and SLI can be explained by a multi-risk model which includes cognitive processes as well as genetic factors.^[30]^[65]^{[non-primary source needed]}

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,^[66]^[67] and may be observed as stuttering, cluttering or hesitant speech.^[22]

Management

Main articles: Management of dyslexia and Dyslexia interventions

There is no cure for dyslexia, but dyslexic individuals can learn to read and write with appropriate educational support. Early intervention is very helpful.

Especially for undergraduates, some consideration of what 'reading' is and its purpose can be useful. There are techniques (reading the first sentence [and/or last] of each paragraph in a chapter, for example) which can give an overview of content. This can be sufficient for some purposes.^{[original research?]} Since stress and anxiety are contributors to a dyslexic's weaknesses in absorbing information, removing these can assist in improving understanding. When a dyslexic knows that not every reading experience must be onerous, it greatly helps their mental approach to the task.

The best approaches acknowledge that the objective in helping to improve a dyslexic's 'reading' is not to 'read-like-a-non-dyslexic-does', but to find a way of extracting information from text that works efficiently for someone who processes such information differently from the majority.

For dyslexia intervention with alphabet writing systems the fundamental aim is to increase a child's awareness of correspondences between graphemes and phonemes, and to relate these to reading and spelling. It has been found that training focused towards visual language and orthographic issues yields longer-lasting gains than mere oral phonological training.^[68]

Context sensitive spell checkers combined with text-to-speech systems offer forms of assistive technology to dyslexia users, supporting reading and writing.

There is some evidence that the use of specially tailored fonts may provide some measure of assistance for those suffering from dyslexia; however scientific confirmation of this currently appears to be limited to a single master's thesis.^[69]^[70] Intervention early on while language areas in the brain are still developing is most successful in reducing long term impacts of dyslexia^[71].

History

Main article: History of developmental dyslexia

Identified by Oswald Berkhan in 1881,^[72] the term 'dyslexia' was later coined in 1887 by Rudolf Berlin,^[73] an ophthalmologist practising in Stuttgart, Germany,^[74] from the Greek prefix δυσ- (dus-), "hard, bad, difficult"^[75] + λέξις (lexis), "speech, word".^[76]^[77]
In 1896, W. Pringle Morgan published a description of a reading-specific learning disorder in the British Medical Journal titled "Congenital Word Blindness".^[78]
During the 1890s and early 1900s, James Hinshelwood published a series of articles in medical journals describing similar cases of congenital word blindness. In his 1917 book Congenital Word Blindness, Hinshelwood asserted that the primary disability was in visual memory for words and letters, and described symptoms including letter reversals, and difficulties with spelling and reading comprehension.^[79]
1925 Samuel T. Orton determined that there was a syndrome unrelated to brain damage that made learning to read difficult. Orton's theory strephosymbolia described individuals with dyslexia having difficulty associating the visual forms of words with their spoken forms.^[80] Orton observed that reading deficits in dyslexia did not seem to stem from strictly visual deficits.^[81] He believed the condition was caused by the failure to establish hemispheric dominance in the brain.^[82] Orton later worked with the psychologist and educator Anna Gillingham to develop an educational intervention that pioneered the use of simultaneous multisensory instruction.^[83]
In contrast, Dearborn, Gates, Bennet and Blau considered a faulty guidance of the seeing mechanism to be the cause. They sought to discover if a conflict between spontaneous orientation of the scanning action of the eyes from right to left and training aimed at the acquisition of an opposite direction would allow an interpretation of the facts observed in the dyslexic disorder and especially of the ability to mirror-read.
1949 Research conducted under G. Mahec show that 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.
1968 Makita suggested that dyslexia was mostly absent among Japanese children.^[84] A 2005 study shows that Makita's claim of rarity of incidence of reading disabilities in Japan to be incorrect.^[85]
In the 1970s a new hypothesis emerged: that dyslexia stems from a deficit in phonological processing or difficulty in recognizing that spoken words are formed by discrete phonemes. Affected individuals have difficulty associating these sounds with the visual letters that make up written words. Key studies suggested the importance of phonological awareness,^[86]
1979 Galaburda and Kemper,^[87] and Galaburda et al. 1985,^[88] reported observations from the examination of post autopsy brains of people with dyslexia. Their studies reporting observed anatomical differences in the language center in a dyslexic brain, taken with the similar work of Cohen et al. 1989,^[89] suggested abnormal cortical development, which was presumed to occur before or during the sixth month of foetal brain development.^[24]
1993 Castles and Coltheart describe developmental dyslexia as two prevalent and distinct varieties using the subtypes of Alexia, Surface and Phonological Dyslexia.^[23] Manis et al. 1996, concluded that there were probably more than two subtypes of dyslexia, which would be related to multiple underlying deficits.^[90] Cestnick and Coltheart (1999) demonstrated what these underlying deficits are in part, through unveiling different profiles of phonological versus surface dyslexics.^[27] Cestnick and Jerger (2000)^[28] and Cestnick (2001)^[29] further demonstrated distinct processing differences between phonological and surface dyslexics.
1994 From post autopsy specimens Galaburda et al., reported: Abnormal auditory processing in people with dyslexia suggests that accompanying anatomical abnormalities might be present in the auditory system. Supported the reported behavioral findings of a left hemisphere-based phonological defect in dyslexic individuals.^[91]
The development of neuroimaging technologies during the 1980s and 1990s enabled dyslexia research to make significant advances. Positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) studies have revealed the neural signature of adult normal reading (e.g. Fiez and Petersen, 1998;^[92] Turkeltaub et al., 2002^[93] and phonological processing (e.g., Gelfand and Bookheimer, 2003;^[94] Poldrack et al., 1999).^[95] Employing various experimental approaches and paradigms (e.g., the detection or judgment of rhymes, nonword reading, and implicit reading), these studies have localized dysfunctional phonological processing in dyslexia to left-hemisphere perisylvian regions, especially for the alphabetic writing system (Paulesu et al., 2001; for review, see Eden and Zeffiro, 1998,^[96]). 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).^[97]
1999 Wydell and Butterworth reported the case study of an English-Japanese bilingual with monolingual dyslexia.^[52] Suggesting that any language where orthography-to-phonology mapping is transparent, or even opaque, or any language whose orthographic unit representing sound is coarse (i.e. at a whole character or word level) should not produce a high incidence of developmental phonological dyslexia, and that orthography can influence dyslexic symptoms.
2003 Ziegler and colleagues claimed that the dyslexia suffered by German or Italian dyslexics is very similar to the one suffered by English dyslexics (readers of different—shallow versus deep orthographic systems), supporting the idea that the origin of dyslexia is mostly biological.^[98]
2007 Lyytinen et al. Researchers are seeking a link between the neurological and genetic findings, and the reading disorder.^[68]
2008 S Heim et al. in a paper titled "Cognitive subtypes of dyslexia" describe how they compared different sub-groups of dyslexics in comparison with a control group. This is one of the first studies not to just compare dyslexics with a non dyslexic control, but to go further and compared the different cognitive sub groups with a non dyslexic control group.^[10]
2008 Wai Ting Siok et al. in a paper titled "A structural–functional basis for dyslexia in the cortex of Chinese readers" describe how dyslexia is language dependent, and especially between alphabetic and non-alphabetic writing systems.^[51]
2010 KK Chung et al. investigated the "Cognitive profiles of Hong Kong Chinese adolescents with dyslexia".^[13]

Society and culture

This section requires expansion.

Education law

There are many different national legal statutes and different national special education support structures with regard to special education provision which relate to the management of dyslexia.

Film, television, and literature

Main article: List of artistic depictions of dyslexia

There have been a number of films, television programs, and works of fiction which focus on the topic of dyslexia.

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.^[26]^[99]^[100]^[101]^[102]

Neuroimaging

For more details on this topic, see Neurological research into dyslexia.

Modern neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) have produced clear evidence of structural differences in the brains of children with reading difficulties. It has been 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.^[103]

That dyslexia is neurobiological in origin is supported by what Lyon et al. proclaimed as "overwhelming and converging data from functional brain imaging investigations" (2003, p. 3). The results of these studies suggest that there are observable differences in how the dyslexic brain functions when compared to the brain of a typical reader. Using fMRI, Shaywitz found that good readers show a consistent pattern of strong activation in the back of the brain with weaker activation in the front of the brain during reading tasks. In contrast, the brain activation pattern in dyslexics is the opposite during reading tasks—the frontal part of the brain becomes overactive with weaker activation in the back. Shaywitz points out "It is as if these struggling readers are using the systems in the front of the brain to try to compensate for the disruption in the back of the brain."^[104]

Fluent word identification in reading is related to the amount of activity in the Left hemisphere posterior system^[105]. In dyslexia the posterior system is often disrupted^[106]. As mentioned above, in order to compensate for lower activity in the posterior system people with dyslexia rely more on the inferior frontal and right hemisphere regions^[107].

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,^[108] with some implication that the observed neural manifestation of developmental dyslexia is task-specific (i.e., functional rather than structural).^[109]

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.^[51] The study focused on comparing children that were raised reading English and children raised reading Chinese. This is supported in a review by T. Hadzibeganovic et al. (2010).^[110]

A University of Maastricht (Netherlands) study revealed that adult dyslexic readers underactivate superior temporal cortex for the integration of letters and speech sounds.^[111]

White matter organization and right prefrontal activity can predict future gain in reading ability^[112]. Greater right prefrontal activity during reading tasks has been associated with reading improvement later in life^[113]. Language training has been shown to improve neural mechanisms of selective auditory attention of children with learning disabilities^[114].

Genetic

High genetic concordance found in twin studies suggest a significant genetic influence on reading ability ^[115] ^[116] , although the degree depends on the definition of dyslexia ^[117]. 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. ^[118] Several genes have been linked to dyslexia, including DCDC2^[119]^[120] and KIAA0319^[119]^[121] on chromosome 6,^[18]^[122] and DYX1C1 on chromosome 15.^[18]^[119], ROBO1^[123], DYX3^[124], the language-disorder candidate gene CMIP^[125], and several others. However, these genes account for a small proportion of variance in reading disability, often less than 0.5%.^[126]^[127] Additionally, the findings are not always replicated. 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.^[128]

It 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. ^[129] The Generalist Genes Hypothesis supports the findings that many learning disabilities are comorbid, such as speech sound disorder, language impairment, and reading disability ^[130]; although this is also influenced by diagnostic overlap.

Many of the genes implicated in dyslexia play a role in general neural development. For example, dyslexia candidate genes DYX1C1, ROBO1 KIAA0319, and DCDC2 appear to be involved in neuronal migration^[131] ^[132]^[133] ^[134]. Animal models are especially useful in determining the function of these genes. For example, Gene knockdown in utero of DYX1C1 disrupts hippocampal development and causes impairments in auditory processing and spatial learning in rodents^[135] and mutations in DCDC2 impairs visuo-spatial memory, visual discrimination, and long-term memory in mice^[136]. The role of neuronal migration in dyslexia is reviewed in Galaburda (2005). ^[137]

Gene x Environment

For more details on Gene x Environment, see Gene–environment interaction.

Research has examined gene x environment interactions in reading disability through twin studies, which estimate the proportion of variance associated with environment and the proportion associated with heritability. If the proportion of one increases, the other must decrease, because they sum to 1. Studies examining the influence of environmental factors such as parental education ^[138], and teacher quality ^[139] have determined that genetics influence phenotype much more in supportive environments than less-optimal environments, supporting the bioecological model of gene x environment interactions. However, this does not rule out the possibility that the diathesis-stress model, which proposes that a phenotype depends on a genetic predisposition in combination with a certain environmental stressor, also occurs. An excellent review of the analysis and interpretation of gene x environment interactions, as well as a review of these interactions in reading disability can be found in Pennington et al. 2009. As stated in this review, "it would be a mistake to consider the diathesis-stress and bioecological models simple opposites of each other, because the nature of the underlying process in each is different (Rutter, 2006). In a diathesis-stress interaction found with molecular methods, we assume that both the diathesis and the stress affect the same specific biological substrate and that the two may be jointly necessary for the phenotype to be observed….In contrast, a bioecological interaction found with either molecular or behavioral genetic methods can occur just because a variety of environmental risk factors have been reduced in a favorable environment, and therefore the environment will contribute less to individual differences, and genes will contribute more. Unlike in a diathesis-stress interaction, the environmental factor in a bioecological interaction does not necessarily act on the same biological substrate as the genetic risk factors. 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." ^[140]

As environment plays a large role in learning and memory^[141] , 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.

Controversy

For more details on Controversy, see Dyslexia research.

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".^[142]

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".

References

^ ^a ^b "Dyslexia Information Page". National Institute of Neurological Disorders and Stroke. 12 May 2010. http://www.ninds.nih.gov/disorders/dyslexia/dyslexia.htm. Retrieved 5 July 2010.
^ Grigorenko EL (January 2001). "Developmental dyslexia: DISLEXIA! an update on genes, brains, and environments". JDYSLEXIA THE SWEET Child Psychol Psychiatry 42 (1): 91–125. doi:10.1111/1469-7610.00704. PMID 11205626. http://www.ingentaconnect.com/content/bpl/jcpp/2001/00000042/00000001/art00005.
^ Schulte-Körne G, Warnke A, Remschmidt H (November 2006). "[Genetics of dyslexia]" (in German). Z Kinder Jugendpsychiatr Psychother 34 (6): 435–44. doi:10.1024/1422-4917.34.6.435. PMID 17094062.
^ 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.
^ 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. http://www.springerlink.com/content/m31740417111l8w3/?p=e21d91f12abf440186aa325a73b0c59dπ=1. Retrieved 11 July 2010.
^ McCandliss BD, Noble KG (2003). "The development of reading impairment: a cognitive neuroscience model". Ment Retard Dev Disabil Res Rev 9 (3): 196–204. doi:10.1002/mrdd.10080. PMID 12953299.
^ ^a ^b Czepita D, Lodygowska E (2006). "[Role of the organ of vision in the course of developmental dyslexia]" (in Polish). Klin Oczna 108 (1–3): 110–3. PMID 16883955.
^ ^a ^b Birsh, Judith R. (2005). "Research and reading disability". In Judith R. Birsh. Multisensory Teaching of Basic Language Skills. Baltimore, Maryland: Paul H. Brookes Publishing. p. 8. ISBN 978-1-55766-676-5. OCLC 234335596.
^ 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.
^ ^a ^b Heim S, Tschierse J, Amunts K (2008). "Cognitive subtypes of dyslexia". Acta Neurobiologiae Experimentalis 68 (1): 73–82. ISSN 0065-1400. PMID 18389017. http://www.ane.pl/linkout.php?pii=6809.
^ 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.
^ 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.
^ ^a ^b ^c 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. http://www3.interscience.wiley.com/journal/122462213/abstract.
^ Handler SM, Fierson WM, Section on Ophthalmology, et al. (March 2011). "Learning disabilities, dyslexia, and vision.". Pediatrics 127 (3): e818–56. doi:10.1542/peds.2010-3670. PMID 21357342.
^ Human Voice Recognition Science Magazine July 2011
^ "Literacy development in successful men and women with dyslexia". Annals of Dyslexia 40 (1): 311–346. 1998. http://nic-nac-project.de/~davison/revFink98.html.
^ Ferrer E, Shaywitz BA, Holahan JM, Marchione K, Shaywitz SE (January 2010). "Uncoupling of reading and IQ over time: empirical evidence for a definition of dyslexia". Psychol Sci 21 (1): 93–101. doi:10.1177/0956797609354084. PMID 20424029.
^ ^a ^b ^c Bishop DV (March 2009). "Genes, cognition, and communication: insights from neurodevelopmental disorders". Ann. N. Y. Acad. Sci. 1156: 1–18. doi:10.1111/j.1749-6632.2009.04419.x. PMC 2805335. PMID 19338500. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2805335.
^ "What Is Dyslexia?". AVKO Education Research Foundation. http://www.avko.org/Info/dyslexia/what_is_dyslexia.htm. Retrieved 5 July 2010.
^ "Developmental reading disorder". MedlinePlus Medical Encyclopedia. 15 October 2008. http://www.nlm.nih.gov/medlineplus/ency/article/001406.htm. Retrieved 5 July 2010.
^ "Developmental dyslexia in adults: a research review". National Research and Development Centre for Adult Literacy and Numeracy. 1 May 2004. pp. *133–147. http://www.nrdc.org.uk/projects_details.asp?ProjectID=75. Retrieved 13 May 2009.
^ ^a ^b ^c Brazeau-Ward, Louise (2001). Dyslexia and the University. Canada: Canadian Dyslexia Centre. pp. 1–3. ISBN 1-894964-71-3. http://www.dyslexiaassociation.ca/english/files/universityanddyslexia.pdf.
^ ^a ^b 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.
^ ^a ^b ^c ^d 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. http://brain.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=11099442.
^ Boder E (October 1973). "Developmental dyslexia: a diagnostic approach based on three atypical reading-spelling patterns". Developmental Medicine and Child Neurology 15 (5): 663–87. doi:10.1111/j.1469-8749.1973.tb05180.x. PMID 4765237.
^ ^a ^b Galaburda AM, Cestnick L (February 2003). "[Developmental dyslexia]" (in Spanish; Castilian). Rev Neurol 36 Suppl 1: S3–9. PMID 12599096.
^ ^a ^b Cestnick Laurie, Coltheart M, (March 1999). "The Relationship Between Language-Processing and Visual-Processing Deficits in Developmental Dyslexia". Cognition 71 (3): 231–55. doi:10.1016/S0010-0277(99)00023-2. PMID 10476605.
^ ^a ^b 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. PMID 11057735.
^ ^a ^b 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.
^ ^a ^b ^c ^d Huc-Chabrolle M, Barthez MA, Tripi G, Barthélémy C, Bonnet-Brilhault F (April 2010). "[Psychocognitive and psychiatric disorders associated with developmental dyslexia: A clinical and scientific issue]" (in French). Encephale 36 (2): 172–9. doi:10.1016/j.encep.2009.02.005. PMID 20434636.
^ Schott GD, Schott JM (December 2004). "Mirror writing, left-handedness, and leftward scripts". Arch. Neurol. 61 (12): 1849–51. doi:10.1001/archneur.61.12.1849. PMID 15596604. http://archneur.ama-assn.org/cgi/content/full/61/12/1849.
^ Schott GD (January 2007). "Mirror writing: neurological reflections on an unusual phenomenon". J. Neurol. Neurosurg. Psychiatr. 78 (1): 5–13. doi:10.1136/jnnp.2006.094870. PMC 2117809. PMID 16963501. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2117809.
^ Cherry RS, Kruger B (April 1983). "Selective auditory attention abilities of learning disabled and normal achieving children". Journal of Learning Disabilities 16 (4): 202–5. PMID 6864110.
^ Facoetti, Andrea; Nicola Corradi, Milena Ruffino, Simone Gori, Marco Zorzi (27 July 2010). "Visual spatial attention and speech segmentation are both impaired in preschoolers at familial risk for developmental dyslexia". Dyslexia 16 (3): 226–239. doi:10.1002/dys.413. PMID 20680993.
^ Lovio R, Näätänen R, Kujala T (June 2010). "Abnormal pattern of cortical speech feature discrimination in 6-year-old children at risk for dyslexia". Brain Res. 1335: 53–62. doi:10.1016/j.brainres.2010.03.097. PMID 20381471. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6SYR-4YT6D8D-D&_user=10&_coverDate=06%2F04%2F2010&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=37596598eee2566363de236b9a31f630.
^ Ho CS-H, Lai DN-Ch. (1999). Naming-speed deficits and phonological memory deficits in Chinese developmental dyslexia. J Learn Disabil, 2:173–86. doi:10.1016/S1041-6080(00)80004-7
^ Kobayashi MS, Haynes CW, MacAruso P, Hook PE, Kato J (June 2005). "Effects of mora deletion, nonword repetition, rapid naming, and visual search performance on beginning reading in Japanese.". Annals of dyslexia 55 (1): 105–28. doi:10.1007/s11881-005-0006-7. PMID 16107782.
^ Jones MW, Branigan HP, Kelly ML. (2009). "Dyslexic and nondyslexic reading fluency: Rapid automatized naming and the importance of continuous lists". Psychonomic Bulletin & Review 16 (3): 567–572. doi:10.3758/PBR.16.3.567.
^ {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}}
^ Ise E, Schulte-Körne G (June 2010). "Spelling deficits in dyslexia: evaluation of an orthographic spelling training". Ann Dyslexia 60 (1): 18–39. doi:10.1007/s11881-010-0035-8. PMID 20352378.
^ http://www.einsteinmontessori.com/ems.php?category=faqs_about_dyslexia
^ Nicolson RI, Fawcett AJ (September 2009). "Dyslexia, dysgraphia, procedural learning and the cerebellum". Cortex 47 (1): 117–27. doi:10.1016/j.cortex.2009.08.016. PMID 19818437.
^ Eva Germano, Antonella Gagliano, Paolo Curatolo (2010). "Comorbidity of ADHD and Dyslexia". Developmental Neuropsychology 35 (5): 475–493. doi:10.1080/87565641.2010.494748. PMID 20721770. http://pdfserve.informaworld.com/260009__925867416.pdf.
^ Berkhan, O. (February 1885). "Über die Störung der Schriftsprache bei Halbidioten und ihre Ähnlichkeit mit dem Stammeln [About the disorder of written language of half-idiots and their similarity with dislaia]". Archiv für Psychiatrie und Nervenkrankenheiten 16 (1): 78–86. doi:10.1007/BF02227300.
^ Wagner, Rudolph (January 1973). "Rudolf Berlin: Originator of the term dyslexia". Annals of Dyslexia 23 (1): 57–63. doi:10.1007/BF02653841.
^ Berlin R (1884). "Uber Dyslexie [About dyslexia]". Archiv fur Psychiatrie 15: 276–278.
^ Ramus F, Rosen S, Dakin SC (April 2003). "Theories of developmental dyslexia: insights from a multiple case study of dyslexic adults". Brain 126 (4): 841–65. doi:10.1093/brain/awg076. PMID 12615643. http://brain.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=12615643.
^ Nicolson RI, Fawcett AJ (April 2007). "Procedural learning difficulties: reuniting the developmental disorders?". Trends Neurosci. 30 (4): 135–41. doi:10.1016/j.tins.2007.02.003. PMID 17328970.
^ Henry, Marcia K. (2005). "The history and structure of the English language". In Judith R. Birsh. Multisensory Teaching of Basic Language Skills. Baltimore, Maryland: Paul H. Brookes Publishing. p. 154. ISBN 978-1-55766-676-5. |oclc=234335596
^ ^a ^b Seki A, Kassai K, Uchiyama H, Koeda T (March 2008). "Reading ability and phonological awareness in Japanese children with dyslexia". Brain Dev. 30 (3): 179–88. doi:10.1016/j.braindev.2007.07.006. PMID 17720344.
^ ^a ^b ^c ^d Siok WT, Niu Z, Jin Z, Perfetti CA, Tan LH (April 2008). "A structural-functional basis for dyslexia in the cortex of Chinese readers". Proc. Natl. Acad. Sci. U.S.A. 105 (14): 5561–6. doi:10.1073/pnas.0801750105. PMC 2291101. PMID 18391194. http://www.pnas.org/cgi/pmidlookup?view=long&pmid=18391194.
^ ^a ^b ^c Wydell TN, Butterworth B (April 1999). "A case study of an English-Japanese bilingual with monolingual dyslexia". Cognition 70 (3): 273–305. doi:10.1016/S0010-0277(99)00016-5. PMID 10384738.
^ David Crystal. 1987. The Cambridge encyclopedia of language. Cambridge: Cambridge University Press
^ Anthony Spaeth. 2003, Spet. 8. Minds at risk. TIMEasia September 1 issue
^ Ziegler, J. C.; Perry, C.; Ma-Wtatt, A.; Ladner, D.; Schulte-Korne, G. (2003). "Developmental dyslexia in different languages: Language specific or universal?". Journal of Experimental Child Psychology 86 (3): 169–193. doi:10.1016/S0022-0965(03)00139-5. PMID 14559203.
^ Ramus F, Pidgeon E, Frith U (July 2003). "The relationship between motor control and phonology in dyslexic children". Journal of Child Psychology and Psychiatry, and Allied Disciplines 44 (5): 712–22. doi:10.1111/1469-7610.00157. PMID 12831115.
^ Rochelle KS, Witton C, Talcott JB (February 2009). "Symptoms of hyperactivity and inattention can mediate deficits of postural stability in developmental dyslexia". Experimental Brain Research 192 (4): 627–33. doi:10.1007/s00221-008-1568-5. PMID 18830588.
^ ^a ^b Katz, Jack (14 May 2007). "APD Evaluation to Therapy: The Buffalo Model". AudiologyOnline. https://www.audiologyonline.com/articles/article_detail.asp?article_id=1803. Retrieved 16 May 2009.
^ Ramus F (April 2003). "Developmental dyslexia: specific phonological deficit or general sensorimotor dysfunction?". Current Opinion in Neurobiology 13 (2): 212–8. doi:10.1016/S0959-4388(03)00035-7. PMID 12744976.
^ Moncrieff, Deborah (2 February 2004). "Temporal Processing Deficits in Children with Dyslexia". speechpathology.com (speechpathology.com). http://www.speechpathology.com/articles/article_detail.asp?article_id=59. Retrieved 13 May 2009.
^ Moncrieff, Deborah (23 September 2002). "Auditory Processing Disorders and Dyslexic Children". audiologyonline.com (audiologyonline.com). http://www.audiologyonline.com/articles/article_detail.asp?article_id=369. Retrieved 13 May 2009.
^ Moore DR (2007). "Auditory processing disorders: acquisition and treatment". J Commun Disord 40 (4): 295–304. doi:10.1016/j.jcomdis.2007.03.005. PMID 17467002.
^ Kruk R, Sumbler K, Willows D (January 2008). "Visual processing characteristics of children with Meares-Irlen syndrome". Ophthalmic & Physiological Optics 28 (1): 35–46. doi:10.1111/j.1475-1313.2007.00532.x. PMID 18201334. http://www3.interscience.wiley.com/journal/119401635/abstract.
^ Evans BJ, Busby A, Jeanes R, Wilkins AJ (September 1995). "Optometric correlates of Meares-Irlen syndrome: a matched group study". Ophthalmic & Physiological Optics 15 (5): 481–7. doi:10.1016/0275-5408(95)00063-J. PMID 8524579.
^ Pennington BF, Lefly DL (May 2001). "Early reading development in children at family risk for dyslexia". Child Development 72 (3): 816–33. doi:10.1111/1467-8624.00317. PMID 11405584.
^ Schuele CM (2004). "The impact of developmental speech and language impairments on the acquisition of literacy skills". Ment Retard Dev Disabil Res Rev 10 (3): 176–83. doi:10.1002/mrdd.20014. PMID 15611989.
^ Peterson RL, McGrath LM, Smith SD, Pennington BF (June 2007). "Neuropsychology and genetics of speech, language, and literacy disorders". Pediatr. Clin. North Am. 54 (3): 543–61, vii. doi:10.1016/j.pcl.2007.02.009. PMID 17543909. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6X3J-4NW0PFC-C&_user=10&_coverDate=06%2F30%2F2007&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=05064ef5d70eb47be996a37e63953f0c.
^ ^a ^b Lyytinen, Heikki, Erskine, Jane, Aro, Mikko, Richardson, Ulla (2007). "Reading and reading disorders". In Hoff, Erika. Blackwell Handbook of Language Development. Blackwell. pp. 454–474. ISBN 978-1-4051-3253-4.
^ Nalewicki, Jennifer (31 October 2011). "Bold Stroke: New Font Helps Dyslexics Read". Scientific American. Scientific American, a Division of Nature America, Inc.. http://www.scientificamerican.com/article.cfm?id=new-font-helps-dyslexics-read. Retrieved 31 October 2011.
^ de Leeuw, Renske (December 2010), "Special Font For Dyslexia?" (in English/Dutch) (PDF) (Master’s thesis), University of Twente, pp. 32, archived from the original on 1 November 2011, http://www.ilo.gw.utwente.nl/ilo/attachments/032_Masterthesis_Leeuw.pdf, retrieved 31 October 2011
^ Chenault B, Thomson J, Abbott RD, Berninger VW (2006). "Effects of prior attention training on child dyslexics' response to composition instruction". Developmental Neuropsychology 29 (1): 243–60. doi:10.1207/s15326942dn2901_12. PMID 16390296. 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.
^ Berkhan O (1917). Neur. Zent 28.
^ Wagner, Rudolph (January, 1973). "Rudolf Berlin: Originator of the term dyslexia". Annals of Dyslexia 23 (1): 57–63. doi:10.1007/BF02653841.
^ "Uber Dyslexie". Archiv fur Psychiatrie 15: 276–278.
^ δυσ-, Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus
^ λέξις, Henry George Liddell, Robert Scott, A Greek-English Lexicon, on Perseus
^ dyslexia, Online Etymology Dictionary
^ Snowling MJ (November 1996). "Dyslexia: a hundred years on". BMJ 313 (7065): 1096–7. PMC 2352421. PMID 8916687. http://bmj.com/cgi/pmidlookup?view=long&pmid=8916687.
^ Hinshelwood, James (1917). Congenital Word-blindness. London: H.K. Lewis. OCLC 9713889. http://www.archive.org/details/congenitalwordbl00hinsrich. ^{[page needed]}
^ Orton, Samuel (1925). "Word-blindness in school children". Archives of Neurology and Psychiatry 14 (5): 285–516. http://archneurpsyc.ama-assn.org/cgi/content/summary/14/5/581.
^ 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.
^ Orton, Samuel T. (7 April 1928). "Specific Reading Disability — Strephosymbolia". Journal of the American Medical Association 90 (14): 1095–9.
reprinted: Orton, Samuel T. (December 1963). "Specific reading disability — Strephosymbolia". Annals of Dyslexia 13 (1): 9–17. doi:10.1007/BF02653604.
^ Goeke, Jennifer; Goeke, J. L. (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.
^ 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.
^ "Reading disabilities in modern Japanese children. Takehiko Hirose. 2005; Journal of Research in Reading – Wiley InterScience". http://www3.interscience.wiley.com/journal/119461051/abstract.
^ Bradley, L; Bryant, P. E. (1983). "Categorizing sounds and learning to read—a causal connection". Nature 30 (2): 419–421. doi:10.1038/301419a0.
^ Galaburda AM, Kemper TL (August 1979). "Cytoarchitectonic abnormalities in developmental dyslexia: a case study". Annals of Neurology 6 (2): 94–100. doi:10.1002/ana.410060203. PMID 496415. http://www.scholaruniverse.com/ncbi-linkout?id=496415.
^ 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.
^ 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. http://www.nlm.nih.gov/medlineplus/aphasia.html.
^ 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.
^ Galaburda AM, Menard MT, Rosen GD (August 1994). "Evidence for aberrant auditory anatomy in developmental dyslexia". Proc. Natl. Acad. Sci. U.S.A. 91 (17): 8010–3. doi:10.1073/pnas.91.17.8010. PMC 44534. PMID 8058748. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=44534.
^ Fiez JA, Petersen SE (February 1998). "Neuroimaging studies of word reading". Proc. Natl. Acad. Sci. U.S.A. 95 (3): 914–21. doi:10.1073/pnas.95.3.914. PMC 33816. PMID 9448259. http://www.pnas.org/cgi/pmidlookup?view=long&pmid=9448259.
^ 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.
^ 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.
^ 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. doi:10.1006/nimg.1999.0441. PMID 10385578.
^ 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.
^ Eden GF, Jones KM, Cappell K (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.
^ 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. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WJ9-49S3C95-1&_user=10&_coverDate=11%2F30%2F2003&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=624d7f18f166694ceea379eda46e8755.
^ "Dyslexia assessment in Arabic. Gad Elbeheri. 2006; Journal of Research in Special Educational Needs – Wiley InterScience". http://www3.interscience.wiley.com/journal/118567835/abstract.
^ Smythe I, Everatt J, Al-Menaye N, et al. (August 2008). "Predictors of word-level literacy amongst Grade 3 children in five diverse languages". Dyslexia 14 (3): 170–87. doi:10.1002/dys.369. PMID 18697190.
^ Friedmann N, Rahamim E (September 2007). "Developmental letter position dyslexia". J Neuropsychol 1 (Pt 2): 201–36. doi:10.1348/174866407X204227. PMID 19331018.
^ Schiff R, Raveh M (May 2007). "Deficient morphological processing in adults with developmental dyslexia: another barrier to efficient word recognition?". Dyslexia 13 (2): 110–29. doi:10.1002/dys.322. PMID 17557687.
^ Cao F, Bitan T, Chou TL, Burman DD, Booth JR (October 2006). "Deficient orthographic and phonological representations in children with dyslexia revealed by brain activation patterns". Journal of Child Psychology and Psychiatry, and Allied Disciplines 47 (10): 1041–50. doi:10.1111/j.1469-7610.2006.01684.x. PMC 2617739. PMID 17073983. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2617739.
^ Shaywitz, Sally (2003). Overcoming dyslexia: a new and complete science-based program for reading problems at any level. Vintage Books. p. 81. ISBN 0-679-78159-5.
^ Pugh KR, Mencl WE, Jenner AR, et al. (2000). <207::AID-MRDD8>3.0.CO;2-P "Functional neuroimaging studies of reading and reading disability (developmental dyslexia)". Mental Retardation and Developmental Disabilities Research Reviews 6 (3): 207–13. doi:10.1002/1098-2779(2000)6:3<207::AID-MRDD8>3.0.CO;2-P. PMID 10982498. http://dx.doi.org/10.1002/1098-2779(2000)6:3<207::AID-MRDD8>3.0.CO;2-P.
^ Pugh KR, Mencl WE, Jenner AR, et al. (2000). <207::AID-MRDD8>3.0.CO;2-P "Functional neuroimaging studies of reading and reading disability (developmental dyslexia)". Mental Retardation and Developmental Disabilities Research Reviews 6 (3): 207–13. doi:10.1002/1098-2779(2000)6:3<207::AID-MRDD8>3.0.CO;2-P. PMID 10982498. http://dx.doi.org/10.1002/1098-2779(2000)6:3<207::AID-MRDD8>3.0.CO;2-P.
^ Pugh KR, Mencl WE, Jenner AR, et al. (2000). <207::AID-MRDD8>3.0.CO;2-P "Functional neuroimaging studies of reading and reading disability (developmental dyslexia)". Mental Retardation and Developmental Disabilities Research Reviews 6 (3): 207–13. doi:10.1002/1098-2779(2000)6:3<207::AID-MRDD8>3.0.CO;2-P. PMID 10982498. http://dx.doi.org/10.1002/1098-2779(2000)6:3<207::AID-MRDD8>3.0.CO;2-P.
^ Chertkow H, Murtha S (1997). "PET activation and language". Clinical Neuroscience 4 (2): 78–86. PMID 9059757. http://www.nlm.nih.gov/medlineplus/nuclearscans.html.
^ McCrory E, Frith U, Brunswick N, Price C (September 2000). "Abnormal functional activation during a simple word repetition task: A PET study of adult dyslexics". Journal of Cognitive Neuroscience 12 (5): 753–62. doi:10.1162/089892900562570. PMID 11054918.
^ Hadzibeganovic, Tarik; Maurits van den Noort, Peggy Bosche, Matjaz Perc, Rosalinde van Kralingen, Katrien Mondt and Max Coltheart (2010). "Cross-Linguistic Neuroimaging and Dyslexia: A Critical View". Cortex 46 (10): 1312–6. doi:10.1016/j.cortex.2010.06.011. PMID 20684952. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B8JH1-50GMMRS-1&_nxudi=B8JH1-50GMMRS-4&_rdoc=7&_srch=doc-info%28%23toc%2343685%239999%23999999999%2399999%23FLA%23display%23Articles%29&_user=10&_fmt=high&_orig=browse&_ct=103&_sort=d&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=27144b316a7271c0b170bf7966c54b66. Retrieved 17 July 2010.
^ Blau V, van Atteveldt N, Ekkebus M, Goebel R, Blomert L (March 2009). "Reduced neural integration of letters and speech sounds links phonological and reading deficits in adult dyslexia". Current Biology 19 (6): 503–8. doi:10.1016/j.cub.2009.01.065. PMID 19285401.
^ Hoeft F, McCandliss BD, Black JM, et al. (January 2011). "Neural systems predicting long-term outcome in dyslexia". Proceedings of the National Academy of Sciences of the United States of America 108 (1): 361–6. doi:10.1073/pnas.1008950108. PMC 3017159. PMID 21173250. http://www.pnas.org/cgi/pmidlookup?view=long&pmid=21173250.
^ Hoeft F, McCandliss BD, Black JM, et al. (January 2011). "Neural systems predicting long-term outcome in dyslexia". Proceedings of the National Academy of Sciences of the United States of America 108 (1): 361–6. doi:10.1073/pnas.1008950108. PMC 3017159. PMID 21173250. http://www.pnas.org/cgi/pmidlookup?view=long&pmid=21173250.
^ Stevens C, Fanning J, Coch D, Sanders L, Neville H (April 2008). "Neural mechanisms of selective auditory attention are enhanced by computerized training: electrophysiological evidence from language-impaired and typically developing children". Brain Research 1205: 55–69. doi:10.1016/j.brainres.2007.10.108. PMC 2426951. PMID 18353284. http://linkinghub.elsevier.com/retrieve/pii/S0006-8993(08)00297-7.
^ Wadsworth, SJ; DeFries JC, Olson RK, Willcutt EG. (December 2007). "Colorado longitudinal twin study of reading disability". Ann dyslexia 57 (2): 139–60. doi:10.1007/s11881-007-0009-7. PMID 18060583.
^ Harlaar, N; Spinath FM, Dale PS, Plomin R (April 2005). "Genetic influences on early word recognition abilities and disabilities: a study of 7-year-old twin". J Child Psychol Psychiatry 46 (4): 373–84. doi:10.1111/j.1469-7610.2004.00358.x. PMID 15819646.
^ Olson, RK (2002). "Dyslexia: nature and nurture". Dyslexia 8 (3): 143–159. doi:10.1002/dys.228.
^ Grigorenko EL, Wood FB, Meyer MS (January 1997). "Susceptibility loci for distinct components of developmental dyslexia on chromosomes 6 and 15". American Journal of Human Genetics 60 (1): 27–39. PMC 1712535. PMID 8981944. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1712535.
^ ^a ^b ^c Shastry BS (2007). "Developmental dyslexia: an update". J. Hum. Genet. 52 (2): 104–9. doi:10.1007/s10038-006-0088-z. PMID 17111266.
^ Meng H, Smith SD, Hager K (November 2005). "DCDC2 is associated with reading disability and modulates neuronal development in the brain". Proc. Natl. Acad. Sci. U.S.A. 102 (47): 17053–8. doi:10.1073/pnas.0508591102. PMC 1278934. PMID 16278297. http://www.pnas.org/cgi/pmidlookup?view=long&pmid=16278297.
^ Paracchini S, Steer CD, Buckingham LL (December 2008). "Association of the KIAA0319 dyslexia susceptibility gene with reading skills in the general population". The American Journal of Psychiatry 165 (12): 1576–84. doi:10.1176/appi.ajp.2008.07121872. PMID 18829873.
^ Grigorenko EL, Wood FB, Meyer MS, Pauls DL (February 2000). "Chromosome 6p influences on different dyslexia-related cognitive processes: further confirmation". American Journal of Human Genetics 66 (2): 715–23. doi:10.1086/302755. PMC 1288124. PMID 10677331. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1288124.
^ Hannula-Jouppi, Katariina; Nina Kaminen-Ahola, Mikko Taipale, Ranja Eklund, Jaana Nopola-Hemmi,Helena Kääriäinen, Juha Kere (October 2005). "The Axon Guidance Receptor Gene ROBO1 Is a Candidate Gene for Developmental Dyslexia". The Axon Guidance Receptor Gene ROBO1 Is a Candidate Gene for Developmental Dyslexia 1 (4): 0467–0474. doi:10.1371/journal.pgen.0010050. PMC 1270007. PMID 16254601. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1270007.
^ Fagerheim, T; Raeymaekers P, Tønnessen FE, Pedersen M, Tranebjaerg L, Lubs HA. (September 1999). "A new gene (DYX3) for dyslexia is located on chromosome 2". J Med Genet. 36 (9): 664–9. doi:10.1136/jmg.36.9.664. PMID 10507721.
^ Scerri, TS; Morris AP, Buckingham LL, Newbury DF, Miller LL, Monaco AP, Bishop DV, Paracchini S. (August 2011). DCDC2, KIAA0319 and CMIP are associated with reading-related traits 70 (3): 237–45. doi:10.1016/j.biopsych.2011.02.005. PMID 21457949.
^ Butcher, LM; O S P Davis, I W Craig, and R Plomin (June 2008). "Genome-wide quantitative trait locus association scan of general cognitive ability using pooled DNA and 500K single nucleotide polymorphism microarrays". Genes Brain Behav. 7 (4): 435–46. doi:10.1111/j.1601-183X.2007.00368.x.
^ Meaburn, EL; N Harlaar, I W Craig, L C Schalkwyk, R Plomin (2008). "Quantitative trait locus association scan of early reading disability and ability using pooled DNA and 100K SNP microarrays in a sample of 5760 children". Molecular Psychiatry 13: 729–740. doi:10.1038/sj.mp.4002063.
^ 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. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2597981.
^ 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.
^ 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.
^ Kid, T; Brose K, Mitchell KJ, Fetter RD, Tessier-Lavigne M (1998). "Roundabout controls axon crossing of the CNS midline and defines a novel subfamily of evolutionarily conserved guidance receptors". Cell 92 (2): 205–215. doi:10.1016/S0092-8674(00)80915-0. PMID 9458045.
^ Meng, H; Smith SD, Hager K, Held M, Liu J, Olson RK, Pennington BF, DeFries JC, Gelernter J, O'Reilly-Pol T, Somlo S, Skudlarski P, Shaywitz SE, Shaywitz BA, Marchione K, Wang Y, Paramasivam M, LoTurco JJ, Page GP, Gruen JR (November 2005). "DCDC2 is associated with reading disability and modulates neuronal development in the brain". Proc Natl Acad Sci U S A. 102 (47): 17053–8. doi:10.1073/pnas.0508591102. PMC 1278934. PMID 16278297. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1278934.
^ Wang, Y; Paramasivam M, Thomas A, Bai J, Kaminen-Ahola N, Kere J, Voskuil J, Rosen GD, Galaburda AM, Loturco JJ. (2006). "DYX1C1 functions in neuronal migration in developing neocortex". Neuroscience 123 (2): 515–22. doi:10.1016/j.neuroscience.2006.08.022. PMID 16989952.
^ Paracchini, S; Ankur Thomas2, Sandra Castro3, Cecilia Lai3,4, Murugan Paramasivam2, Yu Wang2, Brendan J. Keating1, Jennifer M. Taylor1, Douglas F. Hacking5, Thomas Scerri1, Clyde Francks1, Alex J. Richardson6, R. Wade-Martins, F. Stein, J. C. Knight, A. J. Copp, J. LoTurco, A. P. Monaco, (April 2006). "The chromosome 6p22 haplotype associated with dyslexia reduces the expression of KIAA0319, a novel gene involved in neuronal migration". Hum. Mol. Genet. 15 (10): 1659–1666. doi:10.1093/hmg/ddl089. PMID 16600991.
^ Threlkeld, SW; McClure MM, Bai J, Wang Y, LoTurco JJ, Rosen GD, Fitch RH. (March 2007). "Developmental disruptions and behavioral impairments in rats following in utero RNAi of Dyx1c1". Brain Res Bull 71 (5): 508–14. doi:10.1016/j.brainresbull.2006.11.005. PMID 17259020.
^ Gabel, LA; Marin I, LoTurco JJ, Che A, Murphy C, Manglani M, Kass S (November 2011). "Mutation of the dyslexia-associated gene Dcdc2 impairs LTM and visuo-spatial performance in mice". Genes Brain Behav. 10 (8): 868–75. doi:10.1111/j.1601-183X.2011.00727.x. PMID 21883923.
^ Galaburda, Albert (2005). "Dyslexia—A molecular disorder of neuronal migration". Annals of Dyslexia 55 (2): 151–165. doi:10.1007/s11881-005-0009-4.
^ Friend A., DeFries J.C., Olson R. K. (November 2008). "Parental Education Moderates Genetic Influences on Reading Disability". Psychol Sci. 19 (11): 1124–1130. doi:10.1111/j.1467-9280.2008.02213.x. PMC 2605635. PMID 19076484. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2605635.
^ Taylor J, Roehrig AD, Soden Hensler B, Connor CM, Schatschneider C. (April 2010). "Teacher quality moderates the genetic effects on early reading on reading disability". Science 328 (5977): 512–14. doi:10.1126/science.1186149. PMC 2905841. PMID 20413504. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2905841.
^ Pennington, BF; McGrath LM, Rosenberg J, Barnard H, Smith SD, Willcutt EG, Friend A, Defries JC, Olson RK. (January 2009). "Gene × Environment Interactions in Reading Disability and Attention-Deficit/Hyperactivity Disorder". Dev Psychol. 45 (1): 77–89. doi:10.1037/a0014549. PMID 19209992.
^ Roth, TL; Roth ED, Sweatt JD (September 2010). "Epigenetic regulation of genes in learning and memory". Essays Biochem 48 (1): 263–74. doi:10.1042/bse0480263. PMID 20822498.
^ 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.

External links

Research papers, articles and media

Organizations

Developmental disorders: Dyslexia and related specific developmental disorders (F80–F83, 315)

General conditions

Speech and language/ communication disorders	Expressive language disorder · Aphasia/Dysphasia (Expressive aphasia, Receptive aphasia) · Landau–Kleffner syndrome · Lisp · Mixed receptive-expressive language disorder

Scholastic skills/ learning disorder	Dyslexia (Alexia (acquired dyslexia), Developmental dyslexia) · Dysgraphia (Disorder of written expression) · Dyscalculia (Gerstmann syndrome)

Motor function	Developmental dyspraxia

Other	Auditory processing disorder · Scotopic sensitivity syndrome

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dyslexia

dys·lex·i·a

dyslexia

Dyslexia

dyslexia

dyslexia

dyslexia

dyslexia

categories related to 'dyslexia'

dyslexia

dyslexia

Dyslexia

Classification

Signs and symptoms

Common Symptoms

Preschool-aged children

Early primary school children

Older primary school children

Secondary school children and adults

Comorbidities

Cause

Effect of language orthography

Cross-cultural prevalence

Exacerbating conditions

Management

History

Society and culture

Education law

Film, television, and literature

Research

Neuroimaging

Genetic

Gene x Environment

Controversy

See also

References

External links

Dyslexia

	dyslexic
	Dyslexia: The Hidden Disability (1988 Education Film)
	The Princess and the Cabbie (1981 Drama Film)

	What is the opposite of dyslexia? Read answer...
	Who gets Dyslexia? Read answer...
	I have many symptoms of dyslexia but can easily read and write. do i have dyslexia? Read answer...

	What is moderate dyslexia?
	Does nilmar have dyslexia?
	How do you beat dyslexia?


Patrick Dempsey