Alexia refers to a reading disorder caused by some form of acquired brain pathology, most commonly a stroke or tumor, in a previously literate subject. In neuropsychology, a distinction is made between central alexia (commonly seen in aphasia) and peripheral alexia (a perceptual or attentional deficit). The prototypical peripheral alexia is alexia without agraphia (pure alexia), where patients can write but are impaired in reading words and letters. Pure alexia is associated with damage to the left ventral occipitotemporal cortex (vOT) or its connections. Hemianopic alexia is associated with less extensive occipital damage and is caused by a visual field defect, which creates problems reading longer words and passages of text. Reading impairment can also arise due to attentional deficits, most commonly following right hemisphere or bilateral lesions. Studying patients with alexia, along with functional imaging studies of normal readers, has improved our understanding of the neurobiological processes involved in reading. A key question is whether an area in the left ventral occipitotemporal cortex is specialized for or selectively involved in word processing, or whether reading relies on tuning of more general purpose perceptual areas. Reading deficits may also be observed in dementia and traumatic brain injury, but often with less consistent deficit patterns than in patients with focal lesions.
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Acquired dyslexia, Alexia without agraphia, Attentional dyslexia, Hemianopic alexia, Neglect dyslexia, Pure alexia, Visual word recognition, Word form area