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Classification and external resources
ICD-10 R48.0
ICD-9 315.02
OMIM 127700
DiseasesDB 4016
MedlinePlus 001406
Patient UK Dyslexia
MeSH D004410
Parietal lobe – dyslexia neuroanatomy(frontal gyrus,temporal cortex not shown) neurological[1]

Dyslexia, also known as alexia[2] or developmental reading disorder,[3] is characterized by difficulty with learning to read and with differing comprehension of language despite normal or above-average intelligence.[4][5] This includes difficulty with phonological awareness, phonological decoding, processing speed, orthographic coding, auditory short-term memory, language skills and verbal comprehension, or rapid naming.[6][7]

Dyslexia is the most common learning difficulty.[8] Some see dyslexia as distinct from reading difficulties resulting from other causes, such as a non-neurological deficiency with hearing or vision, or poor reading instruction.[9][10] There are three proposed cognitive subtypes of dyslexia (auditory, visual and attentional), although individual cases of dyslexia are better explained by specific underlying neuropsychological deficits (e.g., attention deficit hyperactivity disorder, a visual processing disorder) and co-occurring learning difficulties (e.g., dyscalculia and dysgraphia).[11][12] Although it is considered to be a receptive (afferent) language-based learning disability, dyslexia also affects one's expressive (efferent) language skills.[13]


Internationally, dyslexia is designated as a cognitive disorder related to reading and speech. The National Institute of Neurological Disorders and Stroke definition describes it as "difficulty with spelling, phonological processing (the manipulation of sounds), or rapid visual-verbal responding."[5] There are many published definitions, and many of them are purely descriptive or embody causal theories, that encompass a variety of reading skills, deficits and difficulties with distinct causes rather than a single condition.[14]

Acquired dyslexia, alexia, can be caused by brain damage, stroke, and atrophy. Forms of alexia include: surface dyslexia, semantic dyslexia, phonological dyslexia, and deep dyslexia.[15][16] Acquired surface dyslexia arises after brain damage in a previously literate person and results in pronunciation errors that indicate impairment of the lexical route.[17][18] Numerous symptom-based definitions of dyslexia suggest neurological approaches.

Signs and symptoms[edit]

In early childhood, symptoms that correlate with a later diagnosis of dyslexia include delays in speech,[19] letter reversal or mirror writing, difficulty knowing left from right and difficulty with direction,[20][21] as well as being easily distracted by background noise.[22] This pattern of early distractibility is sometimes partially explained by the co-occurrence of dyslexia and attention deficit hyperactivity disorder (ADHD). Although this disorder occurs in approximately 5% of children, 25–40% of children with either dyslexia or ADHD meet criteria for the other disorder.[23][24]

Dyslexic children of school age may exhibit signs such as difficulty identifying or generating rhyming words, or counting syllables in words (which depend on phonological awareness).[25] They may also show signs of difficulty segmenting words into individual sounds or blending sounds to make words (phonemic awareness).[26] Difficulty with word retrieval or with naming things also feature.[27][28] They are commonly poor spellers, which has been called dysorthographia or dysgraphia (orthographic coding). Whole-word guesses and tendencies to omit or add letters or words when writing and reading are considered tell-tale signs.[29]

Problems persist into adolescence and adulthood and may be accompanied by trouble summarizing stories as well as with memorizing, reading aloud, and learning foreign languages. Adult dyslexics can read with good comprehension, although they tend to read more slowly than non-dyslexics and perform worse at spelling and nonsense word reading, a measure of phonological awareness.[30][31]

A common misconception about dyslexia assumes that dyslexic readers all write words backwards or move letters around when reading. In fact this only occurs among half of dyslexic readers.[32]


The complexity of a language's orthography (i.e., its conventional spelling system, see orthographic depth) has a direct impact upon how difficult it is to learn to read that language. English has a comparatively deep orthography within the Latin alphabet writing system, with a complex structure that employs spelling patterns of several levels: principally, letter-sound correspondences, syllables, and morphemes. Other languages, such as Spanish, have mostly alphabetic orthographies that employ letter-sound correspondences, so-called shallow orthographies, making them relatively easy to learn. English, by comparison, presents more of a challenge.[33] Logographic writing systems, notably Japanese and Chinese characters, have graphemes that are not linked directly to their pronunciation, which pose a different type of difficulty to the dyslexic learner.[34][35] Different neurological deficits may cause varying degrees of difficulty in learning one writing system when compared to another, as the neurological skills required to read, write, and spell can vary between systems.[34]

Associated conditions[edit]

Several learning disabilities often occur with dyslexia, but it is unclear whether these learning disabilities share underlying neurological causes with dyslexia.[36] These disabilities include:

  • Dysgraphia – A disorder which expresses itself primarily through writing or typing, although in some cases it may also affect eye–hand coordination, direction- or sequence-oriented processes such as tying knots or carrying out a repetitive task. In dyslexia, dysgraphia is often multifactorial, due to impaired letter writing automaticity, finger motor sequencing challenges, organizational and elaborative difficulties, and impaired visual word form which makes it more difficult to retrieve the visual picture of words required for spelling.[37][38]
  • Attention deficit disorder – A significant degree of comorbidity has been reported between ADHD and dyslexia or reading disorders;[39][40] it occurs in 12–24% of all individuals with dyslexia.[41] Research studying the impact of interference on adults with and without dyslexia has revealed large differences in terms of attention deficits for adults with dyslexia, and has implications for teaching reading and writing to dyslexics in the future.[42]
  • Auditory processing disorder – A condition that affects the ability to process auditory information. Auditory processing disorder is a listening disability.[43][44] It can lead to problems with auditory memory and auditory sequencing. Many people with dyslexia have auditory processing problems[45] 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.[46][47]
  • Developmental coordination disorder – 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.[19][48]


Blurring and doubling are two common types of visual stress experienced by those with dyslexia[49]
Main article: Theories of dyslexia

Researchers have been trying to find the neurobiological basis of dyslexia since it was first identified in 1881.[50] An example of one of the problems dyslexics experience would be seeing letters clearly, this may be due to abnormal development of their visual nerve cells.[51]


In the area of neurological research into dyslexia, modern neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) have produced a correlation between functional and structural differences in the brains of children with reading difficulties. Some individuals with dyslexia show less electrical activation in parts of the left hemisphere of the brain involved in reading, which includes the inferior frontal gyrus, inferior parietal lobule, and middle and ventral temporal cortex.[52] 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,[53] with some implication that the observed neural manifestation of developmental dyslexia is task-specific (i.e., functional rather than structural).[54] fMRIs in dyslexics have provided important data supporting the interactive role of the cerebellum and cerebral cortex as well as other brain structures.[55][56]


Genetic research into dyslexia and its inheritance has its roots in the examination of post-autopsy brains of people with dyslexia.[57][58] When they observed anatomical differences in the language center in a dyslexic brain, they showed microscopic cortical malformations known as ectopias and more rarely vascular micro-malformations, and in some instances these cortical malformations appeared as a microgyrus. These studies and those of Cohen et al. 1989[59] suggested abnormal cortical development which was presumed to occur before or during the sixth month of fetal brain development.[60] Abnormal cell formations in dyslexics found on autopsy have also been reported in non-language cerebral and subcortical brain structures.[58][61] MRI data have confirmed a cerebellar role in dyslexia.[62]

Gene–environment interaction[edit]

Research has examined gene–environment interactions in reading disability through twin studies, which estimate the proportion of variance associated with environment and the proportion associated with heritability. Studies examining the influence of environmental factors such as parental education[63] and teacher quality[64] have determined that genetics has greater influence in supportive, rather than less optimal, environments.[65] 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.[65] As the environment plays a large role in learning and memory, it is likely that epigenetic modifications play an important role in reading ability. Animal experiments and measures of gene expression and methylation in the human periphery are used to study epigenetic processes, both of which have many limitations in extrapolating results for application to the human brain.[66]

Dual route hypothesis to reading[67]


The dual-route theory of reading aloud was first described in the early 1970s.[67] This theory suggests that two separate mental mechanisms, or cognitive routes, are involved in reading aloud, with output of both mechanisms contributing to the pronunciation of a written stimulus.[17][68] One mechanism is the lexical route, which is the process whereby skilled readers can recognize known words by sight alone, through a “dictionary” lookup procedure.[67][69] The other mechanism is the nonlexical or sublexical route, which is the process whereby the reader can “sound out” a written word. This is done by identifying the word's constituent parts (letters, phonemes, graphemes) and applying knowledge of how these parts are associated with each other, for example how a string of neighboring letters sound together.[67][69]


Central dyslexias[edit]

Central dyslexias include surface dyslexia, semantic dyslexia, phonological dyslexia, and deep dyslexia.[70][71] ICD-10 reclassified the previous distinction between dyslexia (315.02 in ICD-9) and alexia (315.01 in ICD-9) into a single classification as R48.0. The terms are applied for developmental dyslexia and inherited dyslexia along with developmental aphasia and inherited alexia, which are now read as cognates in meaning and synonymous.[72]

Surface dyslexia[edit]

Main article: Surface dyslexia
Dyslexic brain vs normal brain[73]

In surface dyslexia, words whose pronunciations are 'regular' (highly consistent with their spelling e.g., mint) are read more accurately than words with irregular pronunciation, such as colonel.[74] Difficulty distinguishing homophones is diagnostic of some forms of surface dyslexia.[74] This disorder is usually accompanied by (surface) agraphia and fluent aphasia.[74]

Phonological dyslexia[edit]

Main article: Phonological dyslexia

In phonological dyslexia, patients can read familiar words but have difficulty reading unfamiliar words (such as invented pseudo-words). It is thought that they can recognize words by accessing lexical memory orthographically but cannot 'sound out' novel words. Phonological dyslexia is associated with lesions in varied locations within the territory of the middle cerebral artery. The superior temporal lobe is often also involved. Furthermore, dyslexics compensate by overusing a front-brain section, called Broca's area, associated with aspects of language and speech.[73] Research has pointed towards the theory that phonological dyslexia is a development of deep dyslexia. A treatment for phonological dyslexia is the Lindamood Phoneme Sequencing Program (LiPS). This program is based on a three-way sensory feedback process. The subject uses their auditory, visual, and oral skills to learn to recognize words and word patterns. This is considered letter-by-letter reading using a bottom-up processing technique. Case studies with a total of three patients found a significant improvement in spelling and reading ability after using LiPS.[75]

Deep dyslexia[edit]

See also: Deep dyslexia

Patients with deep dyslexia experience semantic paralexia (para-dyslexia), which happens when the patient reads a word, and says a related meaning instead of the denoted meaning.[74] Deep alexia is more recently seen as a severe version of phonological dyslexia. Deep dyslexia is caused by lesions that are often widespread and include much of the left frontal lobe. Research suggests that damage to the left perisylvian region of the frontal lobe causes deep dyslexia.[74]

Peripheral dyslexias[edit]

Peripheral dyslexias have been described by Bub as "impairment to processes that convert letters on the page into an abstract representation of visual word forms". These include hemianopic dyslexia, neglect dyslexia, attentional dyslexia, and pure dyslexia (also known as dyslexia without agraphia).[71]

Pure dyslexia[edit]

Main article: Pure alexia

Pure dyslexia, also known as agnosic dyslexia, dyslexia without agraphia, and pure word blindness, is dyslexia due to difficulty recognizing written sequences of letters (such as words), or sometimes even letters. It is 'pure' because it is not accompanied by other (significant) language-related impairments. Pure dyslexia does not include speech, handwriting style, language, or comprehension impairments.[76] Pure dyslexia is caused by lesions on the visual word form area (VWFA). The VWFA is composed of the left lateral occipital sulcus and is activated during reading. A lesion in the VWFA stops transmission between the visual cortex and the left angular gyrus. It can also be caused by a lesion involving the left occipital lobe and the splenium of the corpus callosum. It is usually accompanied by a homonymous hemianopsia in the right side of the visual field.[74] Multiple oral re-reading (MOR) is a treatment for pure dyslexia. It is considered a top-down processing technique in which patients read and re-read texts a predetermined number of times or until reading speed or accuracy improves a predetermined amount. The idea behind MOR is to learn how to use context, syntax, and semantics of the text to process written information rather than using bottom-up processing techniques in which letter by letter (LBL) reading is necessary. The theory that the MOR technique only uses top-down processing has been questioned and some studies have shown that in fact, bottom-up processing is in part responsible for reading improvement. This has been proven by reading tests that are engineered to use as few of the same words as possible that are used in training texts during MOR treatment. In these studies, patients did not significantly improve in reading speed or accuracy when reading untrained passages. Untrained passages are defined by having differing vocabulary from the texts used in reading practice. This supports the findings that MOR also has bottom-up processing components.[76]

Hemianopic dyslexia[edit]

Commonly considered to derive from visual field loss due to damage to the primary visual cortex. Sufferers may complain of slow reading but are able to read individual words normally. This is the most common form of peripheral alexia, and the form with the best evidence of the (possibility of) effective treatment.[77]

Neglect dyslexia[edit]

In neglect dyslexia, some letters are neglected (skipped or misread) during reading – most commonly the letters at the beginning or left side of words. This alexia is associated with right parietal lesions. Use of prism glasses in treatment has been demonstrated to produce substantial benefit.[78]

Attentional dyslexia[edit]

People with attentional dyslexia complain of letter crowding or migration, sometimes blending elements of two words into one. Patients perform better when word stimuli are presented in isolation rather than flanked by other words and letters. Using a large magnifying glass may help as this should reduce the effects of flanking interference from nearby words; however, no trials of this or indeed any other therapy for left parietal syndromes have been published.[79]


Woodrow Wilson House dyslexia typewriter[80]

Through compensation strategies and therapy, dyslexic individuals can learn to read and write with educational support.[81] There are techniques and technical aids that can manage or even conceal symptoms of the disorder.[82] Removing stress and anxiety alone can sometimes improve written comprehension.[83] For dyslexia intervention with alphabet writing systems, the fundamental aim is to increase a child's awareness of correspondences between graphemes (letters) and phonemes (sounds), and to relate these to reading and spelling by teaching him or her to blend the sounds into words. It has been found that reinforced collateral training focused towards visual language (reading) and orthography (spelling) yields longer-lasting gains than mere oral phonological training.[84] Intervention early on while language areas in the brain are still developing is most successful in reducing long-term impacts of dyslexia.[85] There is some evidence that the use of specially tailored fonts may provide some measure of assistance for people who have dyslexia.[86][87] Among these fonts are Dyslexie and OpenDyslexic, which were created with the notion that many of the letters in the Latin alphabet are visually similar and therefore confusing for people with dyslexia.[88] Dyslexie, along with OpenDyslexic, put emphasis on making each letter more unique to assist in reading.[88]


The prevalence of dyslexia is unknown and estimates of its prevalence vary greatly, spanning 1–33% of the population.[89] Most prevalence estimates for dyslexia span 5–10% of a given population, although no studies have indicated an exact percentage.[41][90] Internationally, there are differing definitions of dyslexia, but despite the significant differences between the writing systems, Italian, German and English speaking populations suffer similarly from dyslexia.[91] Dyslexia is not limited to difficulty in converting letters into sounds, but Chinese dyslexics have difficulty in extracting shapes of Chinese characters into meanings.[92]


A summary version of the map above,[93] showing predominant forms of writing systems by country and what their characters represent:
  Alphabet (consonants and vowels)
  Abjad (only consonants)
  Abugida (family-related syllables)
  Ideograms (ideas)
  Syllabary (isolated syllables)

Dyslexia was identified by Oswald Berkhan in 1881,[50] but the term dyslexia was coined in 1887 by Rudolf Berlin, who was an ophthalmologist in Stuttgart.[94][95] He used the term to refer to a case of a young boy who had a severe impairment in learning to read and write in spite of showing typical intellectual and physical abilities in all other respects. In 1896, W. Pringle Morgan, a British physician from Seaford, East Sussex, published a description of a reading-specific learning disorder in a report to the British Medical Journal titled "Congenital Word Blindness". This described the case of Percy, a 14 year old boy who had not yet learned to read, yet showed normal intelligence and was generally adept at other activities typical of children that age.[96] Castles and Coltheart describe phonological and surface types of developmental dyslexia (dysphonetic and dyseidetic, respectively) to classical subtypes of alexia which are classified according to the rate of errors in reading non-words.[60][97] The distinction between phonological and surface types is only descriptive, and devoid of any etiological assumption as to the underlying brain mechanisms.[98] Studies have, however, alluded to potential differential underlying brain mechanisms in these populations given performance differences.[99][100]


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, Hebrew, as well as other languages.[98][101]

See also[edit]


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External links[edit]

Dyslexia associations