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Blindness provides an unparalleled opportunity to study plasticity of the nervous system in humans. Seminal work in this area examined the often dramatic modifications to the visual cortex that result when visual input is completely absent from birth or very early in life (Kupers and Ptito, 2014). More recent studies explored what happens to the visual pathways in the context of acquired blindness. This is particularly relevant as the majority of diseases that cause vision loss occur in the elderly. Our lab and others have demonstrated compromised visual pathway integrity in those with peri-natal and acquired blindness (Schoth et al., 2006; Chan et al., 2012; Li et al., 2013; Lee et al., 2014; Dietrich et al., 2015; Ho et al., 2015; Reislev et al., 2015). Additional studies have begun to examine the changes occurring with certain disease states: patients suffering from retinitis pigmentosa, optic neuritis, and glaucoma, all so far demonstrate deterioration of the white matter tract architecture as a function of disease severity (Garaci et al., 2009; Gabilondo et al., 2014; Ohno et al., 2015). This evidence indicates that the visual system as a whole is profoundly susceptible to degeneration even with small amounts of vision loss. On the surface, these investigations appear to have negative implications for vision restoration efforts. Yet, parallel studies which examine the phenomenon of cross-modal plasticity suggest that a remodeling of the central nervous system is possible, such that areas of the brain which have been deprived of normal afferent input are able to reconstitute themselves to be receptive to alternative sensory channels (Merabet and Pascual-Leone, 2010; Kupers and Ptito, 2014). The literature includes several examples of investigations which show that the visual cortex will react to tactile and auditory stimuli in the blind but will be less readily recruited in sighted patients (Merabet and Pascual-Leone, 2010). Moreover, cross-modal interactions have been demonstrated well beyond the traditional “critical period” and into late adulthood, albeit perhaps in a less robust fashion (Sadato et al., 2002; Bedny et al., 2012; Collignon et al., 2013). The notion that the adult brain is still capable of significant structural and functional remodeling after vision loss provides opportunities to restore vision through mechanical or biological means.

Use of sensory substitution devices as a model system for investigating cross-modal neuroplasticity in humans