Temporal processing deficits in letter-by-letter reading by Ingles and Eskes

Abstract

Based on his seminal contributions in 1891 and 1892, Dejerine is widely credited for initiating the investigation of acquired dyslexia. In the first contribution (1891) he described a patient who developed an inability to read and write after suffering an infarction of the left hemisphere. Dejerine designated the disorder “Alexia with Agraphia”; he attributed it to a loss of the “optical images” of words that were presumed to be supported by the angular gyrus. In 1892, Dejerine described a patient who was able to write but could not read what he (and others) had written (Dejerine, 1892). This disorder, variously known as Alexia without Agraphia, Pure Alexia or Agnosic Alexia, has been reported with regularity since the original account. Although subsequent reports have noted aspects of the disorder not emphasized in Dejerine's index case—pure alexia may be associated with surface (Patterson & Kay, 1982) or deep (Buxbaum & Coslett, 1996) dyslexia—the essential features of the disorder were well documented by Dejerine and the syndrome remains quite consistent with respect to its core phenomenology. Similarly, the pathologic substrate of the disorder has proven to be remarkably constant: the vast majority of patients with pure alexia have lesions involving the occipital lobe of the dominant hemisphere and either the forceps major or, less commonly, the splenium of the corpus callosum. The latter component of the lesion interrupts the white matter tracts connecting the visual association cortices of the right and left hemispheres.