Retinal prosthesis for the blind

Most of current concepts for a visual prosthesis are based on neuronal electrical stimulation at different locations along the visual pathways within the central nervous system. The different designs of visual prostheses are named according to their locations (i.e., cortical, optic nerve, subretinal, and epiretinal). Visual loss caused by outer retinal degeneration in diseases such as retinitis pigmentosa or age-related macular degeneration can be reversed by electrical stimulation of the retina or the optic nerve (retinal or optic nerve prostheses, respectively). On the other hand, visual loss caused by inner or whole thickness retinal diseases, eye loss, optic nerve diseases (tumors, ischemia, inflammatory processes etc.), or diseases of the central nervous system (not including diseases of the primary and secondary visual cortices) can be reversed by a cortical visual prosthesis. The intent of this article is to provide an overview of current and future concepts of retinal and optic nerve prostheses. This article will begin with general considerations that are related to all or most of visual prostheses and then concentrate on the retinal and optic nerve designs. The authors believe that the field has grown beyond the scope of a single article so cortical prostheses will be described only because of their direct effect on the concept and technical development of the other prostheses, and this will be done in a more general and historic perspective.     

Psychomotor development in the blind infant

The blind from birth has a slower psychomotor development than the normal child because he must palliate the deficiency of visual information by the development of suppletory senses and integrate these information to the structuration of environment. An early assistance by a multidisciplinary team with an important participation of the family will however permit a harmonious development.     

Two-dot alignment across the physiological blind spot

Three competing hypotheses have been proposed for the cortical representation of the blind spot. These are: (i) the regions surrounding the blind spot maintain their spatial values; (ii) the opposite sides of the blind spot are represented adjacently at the cortex, so that the blind spot is “sewn-up”; and (iii) the blind spot is sewn-up with compensation occurring in the immediate surround of the blind spot, so that spatial values are distorted only in the immediate surround of the blind spot. To distinguish between these hypotheses we used a two-dot alignment task, with the two dots straddling the blind spot at varying dot separations. Thresholds in the two-dot alignment task are limited by the cortical separation of the two dots. When thresholds for alignment across the blind spot are compared with thresholds over intact retina at the same eccentricity, the three hypotheses predict: (i) no change in thresholds; (ii) a lowering of thresholds; and (iii) a lowering of thresholds but only at separations slightly greater than the diameter of the blind spot. Thresoolds across the blind spot were closely similar to thresholds across intact retina. The results do not support a sewing-up (with or without compensation) of the blind spot. Rather, our results are consistent with a preservation of spatial values around the blind spot.     

Temporal dynamics of the Venetian blind effect

When square wave gratings are viewed binocularly with lower luminance or contrast in one eye, the individual bars of the grating appear to rotate around a vertical axis (Venetian blind effect). The effect has typically been thought to occur due to retinal disparities that result from irradiation and, therefore, are entirely entoptic. If so, the visual system should process disparities from a luminance or contrast disparity and a geometric disparity at the same rate. Studies of motion-in-depth using geometric disparities have shown that the visual system is unable to process depth cues when those cues are oscillated at frequencies greater than 5 Hz. By changing contrast (experiments one and two) and geometric (experiment three) disparity cues over time, the present study measured the frequency at which both the perception of motion-in-depth and the perception of depth diminish. The perception of motion-in-depth from contrast disparities decreased near 1.1 Hz (experiments one and four) and the perception of depth from contrast disparities decreased near 1.3 Hz (experiments one, two and four); both of which are lower than the frequency where depth from a geometric disparity diminished (near 4.8 Hz in experiment three). The differences between the dynamics of depth from contrast and geometric disparities suggest that the perception arises from separate neural mechanisms.