Event:

It has been known since the days of Hubel & Wiesel that visual deprivation results in a lack of responsiveness of neurons in the visual cortex to visual stimuli. At the same time, neurons throughout the visual pathways respond to auditory and tactile stimuli. This has been demonstrated first with single-neuron electrophysiology and later with functional neuroimaging (Rauschecker, 1995). Animals and humans blind from birth show a greater extent of cross-modal reorganization than individuals that lose vision later in life. However, it is still largely unknown what the structural basis of this plasticity is and how specifically visual functions are substituted by nonvisual modalities. Using functional magnetic resonance imaging we have demonstrated that the middle occipital gyrus (MOG) in the visual dorsal stream of early blind humans retains its function in spatial localization and is activated in auditory and tactile spatial tasks (Renier et al., 2010). Accuracy of sound localization correlates directly with the strength of MOG activation.Visual-to-auditory substitution devices have been used to demonstrate that cortical areas in the visual ventral stream also retain their function: these areas remain involved in object recognition when stimulated by auditory and tactile "shapes". The results confirm that cross-modal plasticity can restitute perceptual abilities in the blind that resemble vision while nonvisual modalities are used for “seeing”. Structurally, these abilities are supported by activating “visual” cortex via nonvisual inputs that are preserved (i.e., not pruned) during development (Anurova et al., 2013).
Auditory deprivation resulting from loss of hair cells in the inner ear has similar consequences on cortical organization: Tonotopic maps in the auditory cortex are reorganized and distorted by auditory deprivation in a limited frequency band.  
This auditory remapping can be considered as an example of a filling-in process preventing perceptual gaps at the cortical level after peripheral receptor loss. As an undesirable side effect, this remapping leads to disinhibition in neighboring frequency bands (“lesion-edge frequencies”) and to net hyperactivity perceived as tinnitus.
However, we hypothesize that in a subsequent process top-down suppression from fronto-limbic structures can equalize the tinnitus signal, so that most individuals with sensorineural hearing loss do not develop chronic tinnitus (Rauschecker et al., 2010). The exception are individuals with persistent changes in the fronto-limbic system, including the ventral striatum, which are unable to permanently suppress the tinnitus signal in the auditory system (Leaver et al., 2011). These studies demonstrate that modulatory networks outside specific sensory systems contribute eminently to plasticity and brain reorganization after sensory deprivation.