Neuroscientific research has consistently shown more extensive non-visual activity in the visual cortex of congenitally blind humans compared to sighted controls; a phenomenon known as crossmodal plasticity. Whether or not crossmodal activation of the visual cortex retracts if sight can be restored is still unknown. The present study, involving a rare group of sight-recovery individuals who were born pattern vision blind, employed visual event-related potentials to investigate persisting crossmodal modulation of the initial visual cortical processing stages. Here we report that the earliest, stimulus-driven retinotopic visual cortical activity (<100 ms) was suppressed in a spatially specific manner in sight-recovery individuals when concomitant sounds accompanied visual stimulation. In contrast, sounds did not modulate the earliest visual cortical response in two groups of typically sighted controls, nor in a third control group of sight-recovery individuals who had suffered a transient phase of later (rather than congenital) visual impairment. These results provide strong evidence for persisting crossmodal activity in the visual cortex after sight recovery following a period of congenital visual deprivation. Based on the time course of this modulation, we speculate on a role of exuberant crossmodal thalamic input which may arise during a sensitive phase of brain development.

To clarify the role of sensory experience during early development for adult multisensory learning capabilities, we probed audiovisual spatial processing in human individuals who had been born blind because of dense congenital cataracts (CCs) and who subsequently had received cataract removal surgery, some not before adolescence or adulthood. Their ability to integrate audio-visual input and to recalibrate multisensory spatial representations was compared to normally sighted control participants and individuals with a history of developmental (later onset) cataracts. Results in CC individuals revealed both normal multisensory integration in audiovisual trials (ventriloquism effect) and normal recalibration of unimodal auditory localization following audiovisual discrepant exposure (ventriloquism aftereffect) as observed in the control groups. In addition, only the CC group recalibrated unimodal visual localization after audiovisual exposure. Thus, in parallel to typical multisensory integration and learning, atypical crossmodal mechanisms coexisted in CC individuals, suggesting that multisensory recalibration capabilities are defined during a sensitive period in development.

Humans with a transient phase of congenital pattern vision deprivation have been observed to feature prevailing deficits, particularly in higher order visual functions. However, the neural correlates of these prevalent visual impairments remain unclear. To probe different visual processing stages, we measured steady state visual evoked potentials (SSVEPs) generated by luminance flicker stimuli at 6.1 Hz, with superimposed horizontal periodic motion at 2.1 Hz or 2.4 Hz. SSVEP responses at the fundamental and second harmonic of luminance flicker frequency, and at their intermodulation frequencies with motion information, were analyzed. Three groups were tested: (1) 15 individuals who had suffered a lack of pattern vision from birth due to the presence of bilateral total congenital cataracts (CC group), which were surgically removed between 4 months and 22 years of age, (2) 13 individuals with reversed developmental i.e., later developing cataracts (DC group), and (3) normally sighted control participants (SC group; n = 13) matched in age and sex to the CC individuals. SSVEPs at the second harmonic frequency (i.e., 12.2 Hz) and at the intermodulation frequencies (8.2 Hz, and 8.5 Hz) were attenuated in the CC group. In contrast, fundamental frequency responses (i.e., at 6.1 Hz) were not significantly altered in the CC group compared to the control groups (SC and DC groups). Based on previous evidence on the role of striate vs. extrastriate generators of fundamental vs. second harmonics of SSVEPs, these results provide evidence for a stronger experience dependence of extrastriate than striate cortical processing, and furthermore, suggest a sensitive period for the development of putative nonlinear neural mechanisms hypothesized to mediate visual feature binding.

Visual input during the first years of life is vital for the development of numerous visual functions. While normal development of global motion perception seems to require visual input during an early sensitive period, the detection of biological motion (BM) does not seem to do so. A more complex form of BM processing is the identification of human actions. Here, we tested whether identification rather than detection of BM is experience dependent. A group of human participants who had been treated for congenital cataracts (CC; of up to 18 years in duration, CC group) had to identify ten actions performed by human line figures. In addition, they performed a coherent motion (CM) detection task, which required identifying the direction of CM amid the movement of random dots. As controls, developmental cataract (DC) reversal individuals (DC group) who had undergone the same surgical treatment as CC group were included. Moreover, normally sighted controls were tested both with vision blurred to match the visual acuity (VA) of CC individuals [vision matched (VM) group] and with full sight [sighted control (SC) group]. The CC group identified biological actions with an extraordinary high accuracy (on average ∼85% correct) and was indistinguishable from the VM control group. By contrast, CM processing impairments of the CC group persisted even after controlling for VA. These results in the same individuals demonstrate an impressive resilience of BM processing to aberrant early visual experience and at the same time a sensitive period for the development of CM processing.