Can Vision Be Restored for the Blind?
Most blindness is due to the death of photoreceptors in the retina, such as in retinitis pigmentosa and macular degeneration. Another leading cause of blindness is death of retinal ganglion cells from glaucoma. Damage can also occur in the visual pathways to the neocortex, or to the occipital lobe of the neocortex, can produce different kinds of blindness. The strategy for curing blindness depends on where the damage occurred.
The first and best approach to treating blindness is stopping the disease itself. Most retinal degeneration has a genetic basis. Genetic diseases can be treated indirectly (by artificially restoring the biochemistry upset by the genetic anomaly — for example, through medication) or directly (by altering the gene itself through transgenic technology). However, if many of the affected cells have already died, these approaches may not be possible. Other genetic approaches, such as reprogramming some of the remaining cells in the retina to differentiate into the types that have died, or introducing stem cells to replace the lost cells, may be possible.
Other, more artificial approaches to restoring sight may hold promise in the short term. After the retinal photoreceptors have died, the remaining cells in the retina, including the output retinal ganglion cells, appear to continue to be functional (though silent, due to the loss of their input signal). Several approaches are aimed at stimulating retinal ganglion cells directly. These include genetic modification of the ganglion cells to express their own light-absorbing ion channels so that they respond to light directly without photoreceptors. A difficulty of this approach is that the phototransduction efficiency of the retina will be a lot lower than that of the natural retina, so that significant light amplification, which might be damaging to the retina, may be necessary.
Some blind patients have had electronic chips implanted in their retinas that use electrical current to stimulate either the bipolar cells that photoreceptors would normally stimulate, or the output ganglion cells directly. This approach requires a conversion from a camera image to drive current generators in the chip on the retina. The difficulty is stimulating enough ganglion cells individually. Clinically useful vision probably requires at least hundreds of discrete individually modulated stimulation points, whereas current injected into the retina spreads out over a wide area.
Another visual prosthesis approach has been to inject current modulated from a camera image into the visual cortex. Signal injection higher in the visual system is the only viable approach for glaucoma, where the output retinal ganglion cells have died, or in the case of the physical loss of the eyes. However, most neurons in visual cortex are feature selective for lines or edges of a particular orientation or that move in a particular direction, and it isn’t clear what signal to put on which current stimulators in a chip. This is also a potential problem even for retinal stimulators because the human retina, like all mammalian retinas, probably contains at least 20 distinct classes of retinal ganglion cells.
Some totally artificial vision approaches are based on sensory substitution. Several research groups have used an audio signal and trained blind people to recognize objects in the environment using hearing (bats do this via their own ultrasonic chirps). Facsimiles of point-to-point light intensity derived from a camera have been used to vibrate points on the skin, or even electrically stimulate the tongue as a visual prosthesis. These approaches tend to be low resolution, but they can be implemented immediately.