Alexia is an acquired disorder of reading. The word dyslexia, though in some ways equivalent, is often used to denote a range of disorders in people who fail to develop normal reading skills in childhood. Alexia may be described as an acquired dyslexia.
Alexia may be categorized as:

  • Peripheral:
    • A defect of perception or decoding the visual stimulus (written script); other language functions are often intact.
  • Central:
    • A breakdown in deriving meaning; other language functions are often also affected.
      Peripheral alexias include:
  • Alexia without agraphia:
    • Also known as pure alexia or pure word blindness. This is the archetypal peripheral alexia. Patients lose the ability to recognize written words quickly and easily; they seem unable to process all the elements of a written word in parallel. They can still access meaning but adopt a laborious letter-by-letter strategy for reading, with a marked word-length effect (i.e., greater difficulty reading longer words). Patients with pure alexia may be able to identify and name individual letters, but some cannot manage even this ("global alexia"). Strikingly the patient can write at normal speed (i.e., no agraphia) but is then unable to read what they have just written. Alexia without agraphia often coexists with a right homonymous hemianopia, and color anomia or impaired color perception (achromatopsia); this latter may be restricted to one hemifield, classically right-sided (hemiachromatopsia). Pure alexia has been characterized by some authors as a limited form of associative visual agnosia or ventral simultanagnosia.
  • Hemianopic alexia:
    • This occurs when a right homonymous hemianopia encroaches into central vision. Patients tend to be slower with text than single words as they cannot plan rightward reading saccades.
  • Neglect alexia:
    • Or hemiparalexia, results from failure to read either the beginning or end of a word (more commonly the former) in the absence of a hemianopia, due to hemispatial neglect.

The various forms of peripheral alexia may coexist; following a stroke, patients may present with global alexia which evolves to a pure alexia over the following weeks. Pure alexia is caused by damage to the left occipito-temporal junction, its afferents from early mesial visual areas, or its efferents to the medial temporal lobe. Global alexia usually occurs when there is additional damage to the splenium or white matter above the occipital horn of the lateral ventricle. Hemianopic alexia is usually associated with infarction in the territory of the posterior cerebral artery damaging geniculostriate fibers or area V1 itself, but can be caused by any lesion outside the occipital lobe that causes a macular splitting homonymous field defect. Neglect alexia is usually caused by occipito-parietal lesions, right-sided lesions causing left neglect alexia.
Central (linguistic) alexias include:

  • Alexia with aphasia:
    • Patients with aphasia often have coexistent difficulties with reading (reading aloud and/or comprehending written text) and writing (alexia with agraphia, such patients may have a complete or partial Gerstmann syndrome, the so-called "third alexia" of Benson). The reading problem parallels the language problem; thus in Broca’s aphasia reading is labored with particular problems reading function words (of, at) and verb inflections (-ing, -ed); in Wernicke’s aphasia numerous paraphasic errors are made.

    From the linguistic viewpoint, different types of paralexia (substitution in reading) may be distinguished:

  • Surface dyslexia:
    • Reading by sound: there are regularization errors with excep- tion words (e.g., pint pronounced to rhyme with mint), but nonwords can be read; this may be seen with left medial +/− lateral temporal lobe pathology (e.g., infarction, temporal lobe Pick’s disease, late Alzheimer’s disease).
  • Phonological dyslexia:
    • Reading by sight: difficulties with suffixes, unable to read nonwords; left temporo-parietal lobe pathology.
  • Deep dyslexia:
    • The inability to translate orthography to phonology, manifesting as an inability to read plausible nonwords (as in phonological dyslexia), plus semantic errors related to word meaning rather than sound (e.g., sister read as uncle); visual errors are also common (e.g., sacred read as scared). Deep dyslexia is seen with extensive left hemisphere temporo-parietal damage.

The term transcortical alexia has been used to describe patients with Alzheimer’s disease with severe comprehension deficits who nonetheless are able to read aloud virtually without error all regular and exception words.



Benson DF, Ardila A. Aphasia: a clinical perspective. New York: OUP, 1996: 180-211
Binder JR, Mohr JP. The topography of callosal reading pathways: a case control analysis. Brain 1992; 115: 1807-1826
Coslett HB. Acquired dyslexia. In: D’Esposito M (ed.). Neurological foundations of cognitive neuroscience. Cambridge: MIT Press, 2003: 109-127 Farah MJ. Visual agnosia: disorders of object recognition and what they tell us about normal vision. Cambridge: MIT Press, 1995
Leff A. Alexia. Advances in Clinical Neuroscience & Rehabilitation
2004; 4(3): 18,20,22


Cross References

Acalculia; Achromatopsia; Agnosia; Agraphia; Aphasia; Broca’s aphasia; Gerstmann syndrome; Hemianopia; Macula sparing, Macula splitting; Neglect; Prosopagnosia; Saccades; Simultanagnosia; Visual agnosia; Visual field defects; Wernicke’s aphasia