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Abstract
Clinically different forms of amblyopia share as common denominators an inability to form well-defined and focused images in one or both eyes and, in the case of unilateral amblyopia, unequal visual input to the brain. This suggests two amblyopiogenic mechanisms which are effective, individually or in unison, in the various forms of amblyopia. The first is lack of adequate visual stimulation during infancy, causing visual deprivation. The second mechanism is based on abnormal binocular interaction. The clinical evidence and data from the animal laboratory will be reviewed in support of this dual etiological concept of amblyopia. An etiological classification of amblyopia suggested in 1972 on hypothetical grounds can be upheld on the basis of information that has accumulated since that time. Amblyopia is not a static condition but has a strong dynamic component since its severity can be modified by the type of stimulation received by the sound eye. Special emphases is placed in this lecture on this unique feature which is based on binocular interaction and is similar to the inhibition of afferent visual stimulation during suppression.