Silicon Retinal Implants Are Here

Ant was one of the first to write with this news: "CHICAGO -- Illinois scientists said Friday they have successfully implanted silicon microchips beneath human retinas for the first time, a procedure that holds promise for millions of people with failing eyesight. Earlier this week, three patients who lost almost all of their vision from retinitis pigmentosa -- a hereditary condition in which the retina gradually degenerates -- became the first people to have an Artificial Silicon Retina implanted."

Comments

It's not a microchip

[donutello]

It's a photoelectric cell that generates electrical stimulation similar to the kind that a retina would on being struck by light. This is NOT a microchip. There is no processing or logic involved.

The straight dope on this procedure

[orpheus]

The article states that this procedure is only for retinitis pigmentosa, but in the end, it is not a treatment for RP, but an early biocompatibility test. RP is only a useful physiological test bed that renders the patient blind over large areas of the retina, while leaving most of the retinal structure intact. The patient was undoubtedly a research volunteer, and was aware of all this, and should probbaly more properly be coinsdered a 'subject' (but I hate calling patients that).

As you probably recall from elementary school, there are two types of receptors in the eye. Rods handle B/W vision, are more sensitive to light, and are responsible for night and peripheral vision. Cones handle color vision, and are only found in the central areas of the visual field, especially the area of best vision in the eye, fovea centralis. (not to be confused with a nearby region of *no* vision, the macula lutea or 'blind spot' where the optic nerve enters the retina). Simple layman diagrams and links to useful concepts (but not *absolutely* accurate) can be found at:
http://hyperphysics.p hy-astr.gsu.edu/hbase/vision/retina.html
http://hyperphysics .phy-astr.gsu.edu/hbase/vision/rodcone.html
Here's a good anatomical overview of the eye

RP is a group of genetic diseases which cause the rods to degenerate. about ten different mutation have been linked to forms of RP, which can be dominant, recessive, or X-linked. Initially, the patient loses their peripheral vision, beginning in a single region, then gradually spreading. The fovea centralis is the last region to be affected, if ever, because there are few rods in the fovea. It is not clear if loss of sharp central vision is due to 'pure' RP at all, since mutations in some 'RP' genes can cause macular degenerations or other retinal conditions. It appears that the loss of central vision is dependent on the individual's particular mutation.

The retina is laid out in layers, and in very different way that you might imagine. The photo sensors are in the *back* of the retina, and in front of them are several layers of neurons that allow the sensors to integrate (share info between nearby sensors, etc) and in front of that are the blood vessels a snd the neurons that go from the interneurons into the optic nerve, etc. Light passes through all these layers before hitting the rod and cone sensors. The only things that are 'behind' the sensors are the pigmented (choroid) layer, a black layer that absorbs all leftover light to keep it from bouncing around the eye; and the sclera, the tough "white of the eye" that provides support.
[Slides and images]
[Good slide, exlanations, links, but a bit technical]

So why use this implant in RP? Well, by prying apart the layers of the retina as described, the sensors can be placed where the cones used to be, and with a bit of luck, the overlying layers of interconnecting neurons will remain intact (they are presumably unaffected by the rod-destroying mutations, since 'cone' vision is preserved in RP) All this is done in the periphery of the eye, away from the delicate Fovea and macula. Here it can be tested, through the (largely) intact eye, without significantly affecting the patient's remaining natural vision (though there's always some risk)

This implant links into the web of interneurons in the retina, instead of having to be connected to the optic nerve as the native rods and cones do. You can see how this is easier than trying to do delicate neurosurgery on the optic nerve, and then re-training the patient's visual cortex. This is the most 'natural' process for th patient, since all position info is preserved and the preprocessing of the retina is present (ther preprocessing has two purposes: feedback to nearby sensors, which is lost in man-made sensors, and pre-processing of the visual impulses, which is preserved)

However, a low resolution 'pinhead' sensor on the periphery won't help an RP patient at all. In fact, patients sometimes find patchy remnants of peripheral vision distracting and annoying. Clearly this is not a treatment for RP but an early stage biocompatibility test for later work (that is more likely to be useful in other conditions).

Here's a review article on progress and challenges in similar subretinal implant technologies

(Disclaimer: I published some research on retinal layers as an undergrad, but that was almost 20 years ago, and before I went to medical school)

Some Biological Background

[Effugas]

Among (far too many) other interests, human perception is a major fascination of mine. I had the good fortune to take a perception class last quarter, and we studied much of how the visual system functions. Here's a bit of what's going on:

Most of vision is not, in fact, provided by the whole of the retina. The fovea, which is (optimally) the direct point of focus for light reaching the back of the eye, is also about the size of a pinhead--yet, it contains about half of our photoreceptors. We actually see very little of a scene at any given time; our eyes essentially "paint the fovea" with a strip of images in normal viewing and jitter around for focused viewing, such that the brain has a large amount of content to stitch together and the photoreceptors/neurons don't tire from lack of signal change.

We filter out constant signals automatically, like the hum of your PC you just noticed when I brought it up.

What my major concern is, I can't particularly figure out where this implantation is taking place, in terms of thickness. The nerves that actually carry the visual system through the optic nerve to the striate cortex are in front of, not behind, the existing photoreceptors. You've got two layers of nerves sitting in front of the photoreceptors, and they're placing the chip behind? This makes me wonder whether they're trying to stimulate or amplify existing photoreceptor activity--which leads to all sorts of questions regarding intensity, variance, signal matching, and so on. Did they solve the electrical potential problem? Supposedly you can't interface an electrode with a nervous system for too long, or you kill the nerve. Maybe the size of the implant helps here too--it's not impossible to imagine that this little fleck of a chip is being placed among photoreceptors?

Does anybody know more about this system? I'm getting really burnt on stories about interesting tech with no quality links. *sigh*

Yours Truly,

Dan Kaminsky
DoxPara Research
http://www.doxpara.com