Background Children are diagnosed as dyslexic when their reading performance is much below that which could be expected for their educational level and cannot be explained by a sensory, neurological or psychiatric deficit or by a low IQ. Although poo

It is a widely held belief that developmental dyslexia (DD) is a phonological disorder in which readers have difficulty associating graphemes with their corresponding phonemes. In contrast, the magnocellular theory of dyslexia assumes that DD is a visual disorder caused by dysfunctional magnocellular neural pathways. The review explores arguments for and against these theories. Recent results have shown that DD is caused by (1) a reduced ability to simultaneously recognize sequences of letters that make up words, (2) longer fixation times required to simultaneously recognize strings of letters, and (3) amplitudes of saccades that do not match the number of simultaneously recognized letters. It was shown that pseudowords that could not be recognized simultaneously were recognized almost without errors when the fixation time was extended. However, there is an individual maximum number of letters that each reader with DD can recognize simultaneously. Findings on the neurobiological basis of temporal summation have shown that a necessary prolongation of fixation times is due to impaired processing mechanisms of the visual system, presumably involving magnocells and parvocells. An area in the mid-fusiform gyrus also appears to play a significant role in the ability to simultaneously recognize words and pseudowords. The results also contradict the assumption that DD is due to a lack of eye movement control. The present research does not support the assumption that DD is caused by a phonological disorder but shows that DD is due to a visual processing dysfunction.

This paper explores whether the child's visual system is more or less vulnerable than the adult's visual system, whether the capacity of the child's visual system to recover from cerebral blindness exceeds the capacity of the adult's, and which brain structures can mediate visual functions after damage to the geniculostriate visual system. Reports about the development of visual functions in normal and in visually-deprived children and about the recovery of visual functions after incomplete damage to the occipital lobe, unilateral hemispherectomy, and in the absence of both cerebral hemispheres in early life, are reviewed. In addition, 2 new cases are reported. A child (patient 1) is described, who was blindfolded, but had normal visual experience for 2 hours daily between the 24 and the 30 months of age. Despite the daily visual experience, there was an elevation of the luminance difference threshold (LDT) in the periphery of the visual field. An adult patient (patient 2) showed a special mode of "blindsight" that may be present in brain damaged children but that cannot be tested in young children. This patient was always able to detect targets correctly only by "feeling" their presence without actually seeing them. After damage to the geniculostriate system, lost visual functions reappeared in more than half of the children during visual-field training. In many children, the enlargement of the visual field exceeded the enlargement that was reported in hemianopic adults during visual-field training. In rare cases, visual targets were reliably detected in both visual hemifields, even after hemispherectomy.

Purpose. To investigate whether and what kind of visual function is still present in the absence of both cerebral hemispheres.