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Surely, understanding the mechanisms that account for improvement and “slippage” in the acuity of the adult amblyopic eye should be more thoroughly studied
In 1981, David Hubel and Torsten Wiesel were awarded the Nobel Prize in Physiology or Medicine. Their elegant animal models of various deprivation studies in infancy have provided invaluable information to practising ophthalmologists.1,2 Hubel and Wiesel described the potentially irreversible anatomical consequences of early monocular occlusion.3 The profound and specific cellular loss that occurred in layer IVc of the visual cortex and the laminae of the lateral geniculate nucleus subserving the deprived eye was interpreted as a model of form deprivation amblyopia.4 The fact that permanent cellular changes occurred within weeks of initiating occlusion (eyelid closure) in an infant animal prompted ophthalmologists to consider early surgery in the management of congenital cataracts.5,6 That the strategy was successful in some cases of monocular congenital cataracts was seen as clinical validation of Hubel and …