Loss of vision affects millions of people worldwide and poses extraordinary challenges to individuals in a society that relies heavily on sight. Although in recent years the techniques of molecular genetics have led to a rapid identification of a great number of genes involved in visual diseases (see
While pharmacological interventions provide therapeutic solutions to many physiological problems, a pharmacological approach to the mechanisms of blindness has not been discovered. Furthermore, there remains the pervasive question as to how these molecular approaches will actually restore functional vision after it is completely lost in a given individual. Therefore, there are compelling reasons to pursue the development of sophisticated microelectronic prostheses as a viable rehabilitative and therapeutic options to substitute, and ultimately, restore limited, but useful sight. Such assistive devices have already allowed thousands of deaf patients to hear sounds and acquire language abilities and the same hope exists in the field of visual neurorehabilitation.
Essentially all visual prosthesis efforts share a common principle of providing focal electrical stimulation to intact visual structures (including the retina, optic nerve, lateral geniculate nucleus (LGN) and occipital visual cortex), evoking the sensation of discrete points of light called phosphenes. Figure 1 shows the possible perception of phosphenes generated by stimulating simultaneously 3 electrodes arranged as a triangle.
It is expected that the neural plasticity of the visual system can contribute to an ever-improving correlation between the physical world and evoked phosphenes. Figure 2 shows an example. Immediately after implantation, the evoked phosphenes are likely to induce a poor perception of an object (the letter “E” in this example). However, appropriate learning and rehabilitation strategies will contribute to provide concordant perceptions.
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