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Controversy about the visual magnocellular deficit in developmental dyslexics

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  • Cited by (83)

    • Developmental dyslexia: A deficit in magnocellular-parvocellular co-activation, not simply in pure magnocellular activation

      2019, Vision Research
      Citation Excerpt :

      In particular, these results suggest low-level problems in visuo-temporal information processing, as often showed by higher contrast thresholds for the detection and the discrimination of flicker and motion signals (Martin & Lovegrove, 1987; Cornelissen, Richardson, Mason, Fowler & Stein, 1995; Ridder, Borsting, & Banton, 2001; Slaghuis & Ryan, 1999; Hill & Lovegrove, 1993; Eden et al., 1996; Demb, Boynton, Best, & Heeger, 1998; Pammer & Wheatley, 2001; Buchholz & McKone, 2004; Ben-Yehudah, Sackett, Malchi-Ginzberg, & Ahissar, 2001; Laycock, Crewther, & Crewther, 2012). It has been suggested that these visual problems could arise from an inefficient processing within a part of the visual pathway known as the magnocellular stream (Stein, 2001; Stein, Talcott, & Walsh, 2000). The implication of this model is that the response of the visual magnocellular subsystem (M-system), more sensitive to low spatial (SF), high temporal frequencies (TF) and low contrast, should be reduced in dyslexia, whereas the response of the parvocellular subsystem (P-system), more sensitive to high spatial, low TF and color, should be unaffected.

    • Predicting the reading skill of Japanese children

      2017, Brain and Development
      Citation Excerpt :

      Various factors have been purported to play a role in the occurrence of dyslexia. For example, the phonological theory [3], the involvement of attentional mechanism [4], the visual magnocellular deficit [5], deficits in detecting rapidly presented or rapidly changing sensory stimuli [6], and cerebellar impairment [7] have been proposed as the pathophysiology of dyslexia. We believe, however, that the occurrence of dyslexia cannot be explained by a single mechanism.

    • Morphological differences in the lateral geniculate nucleus associated with dyslexia

      2015, NeuroImage: Clinical
      Citation Excerpt :

      Still other critics say that deficits in dyslexia are not generally specific to visual magnocellular functions (Amitay et al., 2002), and several studies have failed to find functional magnocellular differences associated with dyslexia (e.g. Farrag et al., 2002; Vanni et al., 1997; Victor et al., 1993). However, the magnocellular theory does not claim that a magnocellular deficit is the single cause of the disorder, but instead interacts with other factors and might only be a risk factor (Stein et al., 2000). Thus, while our results are consistent with the magnocellular theory of dyslexia, they do not necessarily contradict other theories.

    • Cognitive inhibition in students with and without dyslexia and dyscalculia

      2012, Research in Developmental Disabilities
      Citation Excerpt :

      In these hypotheses, the word-inhibition category of cognitive inhibition contains a phonic factor. Word inhibition in cognitive inhibition also includes a visual factor; weakness in this area is similar to the visual perception hypothesis for dyslexia (Stein, Talcott, & Walsh, 2000; Stein & Walsh, 1997; Talcott et al., 1998). The visual factor of word inhibition in cognitive inhibition is in better condition; this finding is identical to those presented in some recent studies (Brunswick, Martin, & Marzano, 2010; von Károlyi, 2001; von Károlyi, Winner, Gray, & Sherman, 2003; Wang & Yang, 2011).

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