Abstract

As a consequence of congenital blindness, compensatory performance in the intact sensory modalities has been documented in humans in many domains, including auditory and tactile perception, auditory localization, voice and language processing, and memory. Both changes of the neural circuits associated with the intact sensory systems (intramodal plasticity) and an activation of deprived visual cortex (crossmodal plasticity) have been observed in blind humans. Compensation in congenitally blind and late-blind individuals involves partially different neural mechanisms. If sight is restored in patients who were born with dense bilateral cataracts (opaque lenses preventing patterned light to reach the retina), considerable visual recovery has been observed in basic visual functions even after long periods of visual deprivation. Functional recovery has been found to be lower for higher-order visual processes, which has been linked to deficits in the functional specialization of neural circuits. First evidence has suggested that crossmodal plasticity largely retracts after sight restoration but that crossmodal activity does not seem to fully dissolve. In contrast, intramodal adaptations in the auditory system have been observed to persist after sight restoration. Except for predominantly subcortically mediated multisensory functions, many multisensory processes have been found to be altered even many years after sight restoration. On the one hand, research in permanently blind humans has documented a high capability of the human neurocognitive system to adapt to an atypical environment. On the other hand, research in sight recovery individuals who had suffered a transient phase of visual deprivation following birth has demonstrated functional specific sensitive periods in the development of visual and multisensory neural circuits.

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