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Morphological differences in the LGN in dyslexia

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1 Morphological differences in the LGN in dyslexia
Monica Giraldo Chica1,4, John P. Hegarty II2, Keith A. Schneider1,2,3 1Centre for Vision Research, York University – Canada 2Department of Psychological Sciences, University of Missouri – USA 3Department of Biology, York University – Canada 4Department of Medicine, University of Barcelona - Spain Introduction: Dyslexia is a specific learning disability of reading and spelling affecting around 5% of schoolchildren, which cannot be attributed to low intellectual ability or inadequate schooling. The proximal cause lies in a phonological deficit in representing and/or processing speech sounds [1]. Hypothesis: A prevalent theory of dyslexia suggests that deficits in the magnocellular processing stream may account for some symptoms of the disorder [2-4]. Reductions in the size of the magnocellular neurons in the human lateral geniculate nucleus (LGN) have been reported in a post-mortem study [5]. Objective: LGN has not been measured directly in humans with dyslexia. We want to test the hypothesis by measuring the LGN in subjects with dyslexia and controls, because this is the only location where the magnocellular and parvocellular streams are disjoint. Methods: 13 subjects with dyslexia and 13 controls were scanned with a Siemens Trio 3T MRI scanner. Subjects were years old. For each subject, 40 proton density weighted images where acquired with a resolution od 0.75x0.75x1mm. The LGN were traced manually on these mean images by six independent experimenters who were blind to the subjects’ group membership. The median of these masks was calculated in order to create the probability map for each subject. We then measured the volume and location in this maps. Results: The overall volume of the LGN is less in subjects with dyslexia compared to controls. The difference was found to be due to a smaller LGN in the left hemisphere of the first group. We also found that the left LGN has a reduction of 0.1 mm in the anterior-posterior extent (p=0.078). The difference map of left LGN shows that voxels in the tail have higher probability to belong to the LGN of a subject with dyslexia, suggesting that their tail might be longer. Even though the position of both LGN in the brain of controls tend to be very variable, the left LGN of subjects with dyslexia is normally located in approximately the same position (Euclidean distance) in respect of the center of mass of the brain. Other findings: Independently of the group membership, we found that the left LGN is 0.14 mm bigger in the lateral-medial extension (p=0.02), and 0.14 mm smaller in the superior-inferior extension (p=0.01) compared to the right one. Since both extensions compensate, total volume is not significantly different (p=0.98). Conclusions: We observed morphological differences in the left LGN between subjects with dyslexia and controls. We also found that left and right LGN have different morphology in both populations. R L Mean values with standard error for the volume of the LGN. The probability map of each subject was then transformed into a common space and averaged to create a probability distribution of the LGN for each population. In this common space we calculated a standard deviation map to visualize the variation of the LGN within subjects of the same group. And we calculated the probability difference map. Each voxel of this map contains the probability of belonging to the LGN of a subject with dyslexia minus the probability that it belongs to a control. Red (blue) voxels are more probable to belong to a subject with dyslexia (control). Central slices for the average map. LGN P = Parvocellular layers M = Magnocellular layers R L Central slices for standard deviation map. Standard deviations of the distance in each dimension and the total distance (Euclidean). R L Central slices for the difference map. L Significantly different voxels in the central slice of the difference map. All significantly different voxels have higher probability in the map of dyslexia. R L References Katia L, Frank R, Nadege V, Denis S, Anne-Lise G Altered Low-Gamma Sampling in Auditory Cortex Accounts for the Three Main Facets of Dyslexia. Stein J, Vincent W The magnocellular theory of dyslexia. Trends in Neurosciences 20: 147–152. Goswami U A temporal sampling framework for developmental dyslexia. Trends in Cognitive Sciences 15: 3-10. Ramus F, Rosen S, Dakin SC, Day BL, Castellote JM, White S, Frith U Theories of developmental dyslexia: insight from a multiple case study of dyslexic adults. Brain 126: 841–865. Livingstone MS, Rosen GD, Dirlane FW, Galaburda AM Physiological and anatomical evidence for magnocellular defect in developmental dyslexia. PNAS 88:


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