Published June 10, 2015 | Version v1
Journal article Open

An Investigation of the Visual Function of Dyslexic Children

  • 1. Refractive Errors Research Center, School of Paramedical Sciences, Mashhad University of Medical Sciences, Mashhad, Iran, Department of Optometry, School of Paramedical Sciences, Mashhad University of Medical Sciences, Mashhad, Iran
  • 2. Department of Speech Therapy, School of Rehabilitation, Mashhad University of Medical Sciences, Mashhad, Iran
  • 3. Department of Ophthalmology, Razavi Hospital, Mashhad, Iran

Description

Background: Dyslexia is the most common learning disability, accounts for 5 to 17% of the school-aged children. Dyslexia is defined as an impairment in which the child faces difficulties learning, reading and writing relative to IQ.
Objective: The aim of this study was to investigate the central and peripheral visual function in a group of dyslexic children who write from right to left direction.
Materials/Patients and Methods: Twenty dyslexic eyes and 20 normal eyes were examined in this study. The visual examinations consisted of measuring distant and near visual acuity, refraction and visual field evaluation using an Octopus
101 automated perimeter. Foveal sensitivity was also measured with static perimetry, and then kinetic perimetry in two target brightness levels: 15 and 20 dB and data were analyzed by SPSS 17 statistical software.
Results: Dyslexic and normal children of the study population aged from 7 to 10 years with mean age of 8.5. Mean visible surface area at brightness levels of 15 and 20 dB was significantly different between two groups (p<0.001, p=0.001). In addition, inferior hemifield had the most noticeable differences between groups compared to other hemifields. No significant difference was noted between two groups for other examinations such as visual acuity at distance and near, refractive errors and static foveal sensitivity.
Conclusions: Visible surface area was defected in dyslexic children; however, the foveal function was similar to normal individuals. These results support the hypothesis of an impairment of the magnocellular function in dyslexia, whereas the parvocellular pathway is intact.

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