It is hypothesized that infantile strabismus may be caused by a lesion within the motion processing visual system (magnocellular pathway) and is reflected by asymmetric optokinetic nystagmus and subjective movement dysfunction. We have compared motion sensitivity in children with acquired and infantile strabismus to age matched normal controls. There is a strong suggestion in our data that children with infantile strabismus have a deficit in motion sensitivity when compared to children with either acquired strabismus or with normal ocular findings. Magnocellular deficits have also been suggested to play a role in dyslexia. If infantile strabismus is proven to be due to magnocellular abnormalities, then children with infantile strabismus may not only be at risk for amblyopia and loss of binocular vision but also for dyslexia. Our study is designed to define the role of magnocellular function in infantile strabismus and to establish parameters of motion sensitivity in subjects with infantile strabismus as compared to subjects with acquired strabismus and to age matched controls. Further studies will compare the incidence of dyslexia in patients with acquired versus infantile strabismus.
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