The aphakic amblyopia that develops in children after the removal of a cataract is particularly difficult to treat. One reason for the recalcitrance to respond to treatment is the early onset of the deprivation: the developing infant's brain has little opportunity to experience the normal binocular stimulation that is needed for proper development of the visual system. The objectives of this project are to understand the neural bases for this and related disorders and, ultimately, to design treatments for amblyopia that are based on sound scientific knowledge. Systematic studies of infant monkeys with extended wear contact lenses that simulate certain aspects of the visual deprivation experienced by children with an early onset infantile cataract corroborate the clinical findings in children that no schedules of patching, even those that maintain relatively good acuity, are successful at maintaining normal binocular function in these children. The proposed studies are designed specifically to better understand the neural mechanisms involved in the loss of binocular function. The primary probe will be a neurological deficit involving motion processing that is linked to loss of binocular function following neonatal deprivation. A combination of behavioral, electrophysiological and anatomical methods will be used to correlate the behavioral deficits to alterations in specific neural subsystems of the brain and to test specific hypotheses about the underlying neurodevelopmental mechanisms. The results will provide direct information about alterations in the central visual pathways of monkeys following early visual deprivation that can also be extrapolated to human infants with aphakic amblyopia, because of the close similarities between this condition as it occurs naturally in humans and experimentally in our monkeys.
| Smith 3rd, E L; Bradley, D V; Fernandes, A et al. (2001) Continuous ambient lighting and eye growth in primates. Invest Ophthalmol Vis Sci 42:1146-52 |
