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Alexia

  • Antonio R. Damasio
Chapter
Part of the Readings from the Encyclopedia of Neuroscience book series (REN)

Abstract

Alexia is a neurological term of Greek origin [A + Gk lex(is)]. It designates a partial or complete inability to read aloud and to comprehend the meaning of printed material, and is also applied to difficulty in learning how to read. The term is generally synonymous with dyslexia, especially in the British literature where dyslexia is the preferred word. In practice, alexia is often used to mean a complete inability to read and dyslexia denotes a milder or partial form of the defect. When it is used unqualified, alexia stands for the acquired form of reading disability which occurs in a previously literate person as a result of focal brain damage. Acquired alexia impairs the reading of sentences and words; in many cases, it may preclude even the reading of single letters. The most common cause of acquired alexia is stroke, i.e., focal brain damage in the form of infarction or hemorrhage, caused by cerebrovascular disease; however cerebral tumors, inflammatory processes, and head injury, among others, can also cause alexia. There are two major types of acquired alexia: in one the reading disorder is accompanied by agraphia, known as alexia-with-agraphia; in another patients retain the ability to write, known as alexia-without-agraphia, or pure alexia.

Further reading

  1. Coltheart M, Patterson K, Marshall JC (1980): Deep Dyslexia. London: Routledge and Kegan PaulGoogle Scholar
  2. Damasio AR, Damasio H (1983): The anatomic basis of pure alexia. Neurology 33:1573–1583.CrossRefGoogle Scholar
  3. Galaburda AM, Kemper T (1979): Cytoarchitectonic abnormalities in developmental dyslexia: A case study. Ann Neurol 6:94.CrossRefGoogle Scholar
  4. Geschwind N, Behan P (1982): Left-handedness: Association with immune disease, migraine, and developmental learning disorder. Proc Natl Acad Sci USA 79:5097–5100CrossRefGoogle Scholar
  5. Geschwind N (1965): Disconnexion syndromes in animals and man. Brain 88:237–294, 585-644CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1989

Authors and Affiliations

  • Antonio R. Damasio

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