September 2011
Volume 11, Issue 11
Free
Vision Sciences Society Annual Meeting Abstract  |   September 2011
Pronounced visual motion deficits in developmental dyslexia associated with a specific genetic phenotype
Author Affiliations
  • Maria Concetta Morrone
    Department of Physiological Science, University of Pisa and IRCCS Stella Maris, Pisa, Italy
  • Marco Cicchini
    Institute of Neuroscience, CNR, Pisa, Italy
  • Monica Consonni
    Vita-Salute San Raffaele University, Milan, Italy
    Division of Neuroscience San Raffaele Scientific Institute, Milan, Italy
  • Francesca Bocca
    Department of Psychology, Ludwig-Maximilians University, München, Germany
  • Sara Mascheretti
    Vita-Salute San Raffaele University, Milan, Italy
  • Paola Scifo
    Division of Neuroscience San Raffaele Scientific Institute, Milan, Italy
    Nuclear Medicine Department San Raffaele Scientific Institute, Milan, Italy
  • Cecilia Marino
    Molecular Biology Laboratory, Scientific Institute Eugenio Medea, Bosisio Parini, Italy
  • Daniela Perani
    Vita-Salute San Raffaele University, Milan, Italy
    Division of Neuroscience San Raffaele Scientific Institute, Milan, Italy
Journal of Vision September 2011, Vol.11, 428. doi:10.1167/11.11.428
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      Maria Concetta Morrone, Marco Cicchini, Monica Consonni, Francesca Bocca, Sara Mascheretti, Paola Scifo, Cecilia Marino, Daniela Perani; Pronounced visual motion deficits in developmental dyslexia associated with a specific genetic phenotype. Journal of Vision 2011;11(11):428. doi: 10.1167/11.11.428.

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Abstract

Deficits of visual motion have often been reported in developmental dyslexia, but the effects are often small and present only in a sub-population of subjects. We studied motion perception in a selective population of 10 dyslexic subjects with an alteration of the gene DCDC2 (crucial for neural migration during embryogenesis) and correlated the visual perceptual deficit with morphological changes of white matter tracts. All subjects showed a severe deficit in contrast thresholds for discriminating drift direction: 9 out of 10 patients failed to discriminate motion direction for gratings of spatial frequency higher than 2 c/deg (8 Hz, 200 ms exposure). In 6 subjects the deficit was anisotropic for motion direction: for example near normal horizontal motion thresholds but highly compromised for vertical motion. The overall average acuity for motion discrimination was around 2 c/deg (±0.4LU), eight times worse than typical control subjects. All patients showed normal contrast sensitivity for motion of low spatial frequencies (<1 c/deg), and for static stimuli. Diffusion tensor imagining (DTI) revealed significant alteration of fractional anisotropy in several white matter tracts, and the ammount of alteration correlated with the magnitude of the motion deficit. Of particular interest was the strong correlation with the fractional anisotropy of the inferior longitudinal fasciculus, at two positions: one just anterior to MT+ (±40 −20 0) and the other slightly more ventral (±58 −40 −22). These results indicate that the observed motion deficits may reflect abnormalities of the mangocellular pathway and of the innervation of MT+ during development. The frequently reported motion perception abnormality in dyslexia may thus result from alteration of fibre bundles associated with the specific genetic risk factors such as those reported here, rather than being characteristic of the entire dyslexia syndrome.

ERC IDEA: STANIB. 
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