Abstract
Damage of primary visual cortex in mature mammals severely disrupts vision by disconnecting much of the cognitive processing machinery of extrastriate cortex from its source of visual signals in the retina. However, equivalent lesions incurred early in postnatal life unmask a substantial latent flexibility of the brain to minimize the disruption by specific and ordered pathway expansions that bypass the lesion. The expansions shape pathways from retina through thalamus to extrastriate cortex and onto the midbrain into new, useful forms that are retained into adult life. These useful modifications support relatively normal signal processing in a variety of structures and the sparing of certain visually guided behaviors, such as aspects of complex-pattern vision and localizing objects introduced into the visual field. Thus, both the brain and the individual are optimized, in the absence of primary visual cortex, by adaptations for useful interactions with the environment. So far, the repercussions of early visual cortex lesions have been most thoroughly documented in cats, although it is likely on the basis of known repercussions and similarity of visual system organization and developmental sequence, that broadly equivalent repercussions and adaptations occur in monkeys and humans following early lesions of primaiy visual cortex. The knowledge gained has implications for devising therapeutic strategies to attenuate defects in vision induced by cortical lesions.