pared with nonimpaired readers (Shaywitz, B. et al., in press; Brunswick et al., 1999; Rumsey et al., 1997; Shaywitz et al., 1998, submitted; Georgiewa et al., 1999).The involvement of the posterior region centered about the angular gyrus is of particular interest, since this portion of association cortex is considered pivotal in carrying out those cross-modal integrations necessary for reading—that is, mapping the visual percept of the print onto the phonological structures of the language (Benson, 1994; Black and Behrmann, 1994; Geschwind, 1965). Consistent with this study of developmental dyslexia, a large literature on acquired inability to read (alexia) describes neuroanatomic lesions most prominently centered about the angular gyrus (Damasio and Damasio, 1983; Dejerine, 1891; Friedman et al., 1993).
It should not be surprising that both the acquired and the developmental disorders affecting reading have in common a disruption in the neural systems serving to link the visual representations of the letters to the phonological structures they represent. While reading difficulty is the primary symptom in both acquired alexia and developmental dyslexia, associated symptoms and findings in the two disorders would be expected to differ somewhat, reflecting the differences between an acquired and a developmental disorder. In acquired alexia, a structural lesion resulting from an injury, such as stroke or tumor, disrupts a component of an already functioning neural system, and the lesion may extend to involve other brain regions and systems. In developmental dyslexia, as a result of a constitutionally based functional disruption, the system never develops normally so that the symptoms reflect the emanative effects of an early disruption to the phonological system. In either case, the disruption is within the same neuroanatomic system. A number of studies of young adults with childhood histories of dyslexia indicate that although they may develop some accuracy in reading words, they remain slow, nonautomatic readers (Bruck, 1992; Felton et al., 1990).
The model used to study reading and reading disability has now been extended to the study of mathematics and mathematics disability. Though these studies are still in their infancy, the indications are that within the next decade, understanding of the underlying cognitive and neurobiological underpinnings of mathematics disability will be elucidated.
The concept of unexpected underachievement remains the central diagnostic criterion for designating a child as LD. Because the definition of LD in EHA/IDEA provided insufficient criteria for identifying eligible children, in 1977 the Department of Education published guidelines for the identification of an unexpected underachievement, settling on an operational defi-