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Visual-Based Deficits (page 5)

By H.W. Catts|A.G. Kamhi
Pearson Allyn Bacon Prentice Hall

Transient Processing Deficits

Scotopic sensitivity syndrome and problems in eye movements have both been suggested to be the result of more primary deficits in visual processing. Researchers have identified two basic visual processing systems, the transient and sustained systems (Campbell, 1974; Graham, 1980). Each system appears to specialize in the processing of particular visual information. The transient system seems to be especially sensitive to global visual features and is thought to play an important role in guiding eye movement. The sustained system, on the other hand, responds to fine detail and is used in visual feature identification (e.g., letter/word recognition). Both of these systems must operate efficiently to meet the visual perceptual demands of reading.

Lovegrove and his colleagues (Lovegrove, 1992; Lovegrove, Martin, & Slaghuis, 1986) have observed that individuals with RD have significant difficulties on a number of nonverbal visual tasks believed to involve the transient system. They proposed that individuals with RD may have a sluggish transient processing system. The slowed processing of the transient visual system could disrupt parallel operation with the sustained system, which in turn might lead to visual distortions and other visual problems during reading.

Others have also found individuals with RD to have deficits on visual tasks related to transient processing (Cestnick & Coltheart, 1999; Eden et al., 1995; Livingstone, Rosen, Drislane, & Galaburda, 1991; Solman & May, 1990). In addition, these behavioral findings are consistent with reports of recent anatomical and physiological deficits in dyslexia (Eden et al., 1996; Livingstone et al., 1991). Livingstone and colleagues (1991), for example, found in postmortem examinations that dyslexics may have less organized and smaller neurons in the brain regions associated with transient visual processing than do normal individuals. Also, as noted above, Eden and colleagues (1996) reported that dyslexics show less task-related activation in these brain regions.

Although there is some converging support of a transient visual processing deficit in poor readers, more than a few studies have failed to find evidence of these deficits (e.g., Chiappe, Stringer, Siegel, & Stanovich, 2002; Hayduck, Bruck, & Cavanagh, 1992; Hogben, Rodino, Clark, & Pratt, 1995). Some of the conflicting findings across group studies could be the result of these deficits being present only in a subset of poor readers. Thus, the subject composition of a given study could influence its outcome. Consistent with this explanation, Ramus (2003) calculated that only 29 percent of poor readers across a number of recent studies (those that presented individual subject data) had visual processing deficits. Conflicting results could also be due to methodological differences in the way visual processing has been measured across studies. Some have further argued that visual processing deficits might in part be explained by problems in attention or motivation (Stuart, McAnally, & Castles, 2001).

Regardless of the issues concerning conflicting results, the question still remains whether visual deficits, if present, are a sufficient cause of reading disabilities. Some have questioned, for example, how transient deficits themselves could lead to the range of problems seen in children with RD (Skottun, 2000). Also, at least some evidence suggests that transient processing deficits often occur in concert with phonological processing deficits (e.g., Eden et al., 1995). A visually based explanation of reading disabilities would be better supported if a group of children with RD could be identified who have a documented history of visual deficits but no impairments in phonological processing or other known causal factors (Share & Stanovich, 1995).

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