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Alexia (condition)

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Title: Alexia (condition)  
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Subject: Dyslexia, Stroke, Word blindness, List of ICD-9 codes 780–799: symptoms, signs, and ill-defined conditions, Joseph Jules Dejerine, Pure alexia
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Alexia (condition)

Classification and external resources
ICD-10 9 MeSH D004410

Alexia (Alexia from the Greek , privative, expressing negation, and λέξις = "word"), or acquired dyslexia, occurs when damage to the brain causes a patient to lose the ability to read.[1] It is also called word blindness, text blindness or visual aphasia.[2]

Those who suffer from "alexia" and "developmental dyslexia" can have similar difficulties, however, "alexia" refers to an acquired reading disability, where reading ability had previously been developed, usually occurring in adulthood conditions, while "developmental dyslexia" refers to developmental reading disability.[3][4]


There are two groups of alexia.

  • The first or main group is "the central dyslexia" group which includes surface dyslexia, semantic dyslexia, phonological dyslexia, and deep dyslexia.[5][6]
  • The second group, "the peripheral dyslexia" group, includes neglect dyslexia, attentional dyslexia, and pure alexia which is also known as alexia without agraphia.[6]

Classification of alexia depends on the site of anatomic damage and whether agraphia (deficits in writing) and/or aphasia (deficits in oral language) is present.[7] Alexia and agraphia are often associated with aphasia, but it is possible to have alexia and agraphia without aphasia.[7] When aphasia is not present, alexia is categorized as either: 1) alexia without agraphia (pure alexia or word blindness) which is associated with left occipital lobe damage, or 2) alexia with agraphia which is associated with lesions of the left angular gyrus.[7][8]


Alexia typically occurs following damage to the dominant hemisphere of the brain which is usually the left. It can also occur with lesions to the occipital and/or parietal lobes, which are responsible for processing auditory, phonological and visual aspects of language. The region at the junction of occipital and temporal lobes (sometimes called the occipito-temporal junction) coordinates information that is gathered from visual and auditory processing and assigns meaning to the stimulus. Alexia can also occur following damage to the inferior frontal. Damage to these different areas of the cortex result in somewhat different patterns of difficulty in affected individuals. In some cases, a stroke can cause alexia.[1][9]

Alexia without agraphia is classified as a disconnection syndrome which involves a disruption of the communication pathways between the left and right cerebral hemispheres.[8] The right visual cortex receives information from the left side of the visual field, and this information must then be transferred through the posterior commissure and splenium of the corpus callosum to the word form system in the left hemisphere.[8] In people with alexia without agraphia, this transfer of information is interrupted.[8] The presence of agraphia is a result of lesions to the left posterior frontal lobe and left superior parietal lobe.[8]


Alexia may be accompanied by expressive aphasia and/or receptive aphasia (Aphasia the inability to produce or comprehend spoken language). Alexia can also co-occur with agraphia, the specific loss of the ability to produce written language even when other manual motor abilities are intact. In other cases, damage is restricted to areas responsible for input processing. The result is known as pure alexia. In this scenario, an individual's ability to produce written language is spared even though they are unable to understand written text.

Alexia without agraphia can result from a lesion of the left occipital splenium of the corpus callosum.


One patient with damage to areas responsible for visual processing was able to regain the ability to read by using motor processing (tracing the shapes of letters).[10]

Notable cases

Canadian novelist Howard Engel suffered from alexia (sine agraphia) following a stroke in 2000. His case was subsequently publicised by neurologist Oliver Sacks.[11]

See also


Further reading

External links

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