System-wide repercussions and adaptive plasticity: the sequelae of immature visual cortex damage

Damage of primary visual cortex in mature mammals severely disrupts vision by disconnecting much of the cognitive processing mac hinery of extrastriat e cortex from its source of visual signals in the retina. However, equivale nt lesions incurred early in postnatal life unmask a substantial latent fle xibility of the brain to minimize the disruption by specific and ordered pa thway 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 modificat ions support relatively normal signal processing in a variety of structures and the sparing of certain visually guided behaviors, such as aspects of c omplex-pattern vision and localizing objects introduced into the visual fie ld. Thus, both the brain and the individual are optimized, in the absence o f primary visual cortex, by adaptations for useful interactions with the en vironment. So far, the repercussions of early visual cortex lesions have be en most thoroughly documented in cats, although it is likely on the basis o f known repercussions and similarity of visual system organization and deve lopmental sequence, that broadly equivalent repercussions and adaptations o ccur in monkeys and humans following early lesions of primary visual cortex . The knowledge gained has implications for devising therapeutic strategies to attenuate defects in vision induced by cortical lesions.