Cross-modal plasticity: where and how?

Key Points Both young and adult brains show a remarkable capacity to be shaped by environmental input, and to be altered by the deprivation of input in one sensory modality (for example, deafness or blindness). However, different areas and functions show different susceptibilities to such plasticity, and different times during the life span of the individual when they are sensitive to such changes. Plastic changes, such as increases in spine density or neuronal density, can occur in the primary cortices that mediate the spared modalities after sensory deprivation in one modality. These changes might underlie reports of behavioural improvements in the spared modalities and/or might result from increased reliance on these modalities. In humans, it is difficult (but not impossible) to distinguish between changes that result from sensory deprivation (for example, deafness) and those that result from altered linguistic experience (for example, using sign language). Improvements in behaviour tend to involve complex processing rather than simple thresholds. Polymodal association areas of cortex can also become reorganized after sensory deprivation. For example, visual deprivation can lead to increased recruitment of parietal cortex and the superior colliculus by the auditory and somatosensory systems. Few studies have investigated the possible critical periods for such reorganization. Studies in deaf and blind humans indicate that recruitment of polymodal association areas might be associated with improved performance in the spared modalities. The primary cortex that is associated with the deprived modality might also undergo plastic changes, in some cases becoming activated by stimuli in the spared modalities. Such activation might result from the persistence of normally pruned polymodal connections, but has been difficult to show in humans. Cross-modal plasticity might result from a variety of mechanisms. Changes in subcortical connectivity might lead to recruitment of the primary visual cortex by auditory inputs, as in the case of the blind mole rat. Other possible mechanisms include alterations in feedback between cortico-cortical connections and the stabilization of long-range connections, such as those found between the primary visual and auditory cortices in the monkey. An understanding of these mechanisms could help in deciding when to provide sensory implants (such as cochlear implants in the deaf or retinal implants in the blind): although some mechanisms might be available throughout life, others seem to be restricted in their time periods of occurrence and in the types of altered experience that they respond to. For example, changes in subcortical connectivity are less likely to occur in the adult and, if they occur at all, might be observed only after major deafferentation. Changes in cortico-cortical connections, however, might be more amenable to changes throughout life and across a variety of altered experiences. Further understanding of the plastic changes that follow sensory deprivation will help to clarify the role of sensory input in specifying cortical responses and behaviour. Such knowledge will also be important for efforts to restore lost sensory modalities by implants or other techniques.