| Alexia (acquired dyslexia) | |
|---|---|
| Classification and external resources | |
| ICD-10 | R48.0 |
| ICD-9 | 315.01, 784.61 |
| MeSH | D004410 |
Alexia (acquired dyslexia) (Alexia from the Greek ἀ, privative, expressing negation, and λέξις = "word") 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 "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 "dyslexia" refers to developmental reading disability.[3][4]
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There are two groups of alexia.
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][7]
Alexia may be accompanied by expressive and/or receptive 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 results from a left occipital splenium of the corpus callosum lesion.
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).[8]
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