Pure alexia is an acquired form of dyslexia in which the individual cannot read due to an inability to perceive the graphical quality of letters as a representation of a sound. This infliction is deemed “pure” because the individual retains her ability to speak and write. Psychologists sometimes refer to pure alexia as “alexia without agraphia,” (agraphia being the inability to write.)


  • Ability to write a passage but inability to read back the passage.
  • Ability to recognize individual letters as a letter. (N = The Letter N, B = The Letter B)
  • Inability to associate individual letters with a sound. (N = “enn”, B = “bee”)*
  • Inability to read a word as a whole.

*This usually requires training to re-associate the grapheme, or picture of the letter, with the name of the letter. The individual will never be able to associate the grapheme with a phoneme, or sound of the letter.


Pure alexia is the direct result of lesions to the brain, specifically to two areas: the left occipital lobe and the splenium. The splenium is one of the posterior zones of the corpus callosum, which is responsible for communication between the two halves of the brain. (Note: Pure alexia can also occur from damage to the splenium in conjunction with the temporal and parietal lobes, since the parts of the visual cortex innervate these other lobes.)

Left occipital lobe damage usually results in hemianopia on the right side. In other words, individuals with pure alexia tend to have a visual impairment that keeps them from seeing objects on the right hand side.

In addition to the injured occipital lobe, the damaged splenium has a synergetic effect resulting in the specific character of pure alexia. The interesting thing about this sort of damage is that the major language areas of the brain are left in tact. Primarily, there is no damage to Wernicke's area nor Broca's area. Since these lesions do not impair Broca's area, motor speech production proceeds as normal. And, Wernicke's area continues to function properly as the word association engine; pure alexics can continue to make appropriate and intricate word choices fluently during language production.

Infarction, or tissue death, resulting from stroke is the typical cause of pure alexia. Specifically speaking, strokes causing pure alexia occur in the posterior cerebral artery.


Since the major language areas of the brain are still available, psychologists can train pure alexics to read once again. Most suffering with pure alexia will never regain full capacity for reading, in fact they will be left with very limited ability to produce correct meaning associations from visual characters. With training, however, pure alexics can learn to read on a letter-by-letter basis.

Essentially, psychologists coach pure alexics to recognize the meaning of a word without pronouncing the sound, internally or externally. First, the patient must once again become familiar with the alphabet. They learn to associate "m" with the fact that it is "the letter m," and without having to understand that it produces the sound "emm," for that ability is no more. Consider the word "money." The patient begins with the letter "m" and then recognizes that letter as "the letter m." Then, the patient considers the letter "o," and recognizes that letter as "the letter o." Once the patient reaches the end of the word, they will realize that the word is "money," and will think of all the things that money reminds them of. Pure alexics will never be able to achieve fluid reading.

You can tell that a pure alexic trained to read letter-by-letter is actually perceiving one letter at a time because word length will increase the time it takes to read the word at a constant linear slope. This means that the time between to perceive each letter is constant. Readers without pure alexia perceive words faster because they can graphically associate the shape of the words themselves, as well as the shape of the individual letters, with the sound they produce.


J.R. Hanley, J. Kay, Reading speed in pure alexia, Neuropsychologia 34 (12) (1996) pp. 1165-1174.