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Eye Transplant Enables Blind Boy to See
Chris Gondek points to this story carried by the Sydney Morning Herald, excerpting: "A one-year-old Pakistani boy saw the world for the first time yesterday through an eye donated by an Indian. Mohammed Ahmed gained partial vision after a difficult operation at the Agarwal Eye Institute in the southern city of Madras. Doctors said Ahmed, who was born blind, would get near-normal sight by the time he heads back to Karachi next week."
The title is very misleading and is born of sloppy reporting. The whole eye was NOT transplanted, rather the cornea was what was transplanted. The cornea had adhered to the boys iris clouding his vision. Technically and surgically, this is nothing of note as corneal replacements have been happening now for years and years. Politically however stuff like this is good for Indian Pakistani relations.
The title suggests that the whole eye was transplanted which would indeed be very exciting as I myself work in vision rescue focusing on diseases that cause blindness through degeneration of the retina. However, the concept of rescuing vision once we have lost it due to trauma to the retina or degenerative diseases is much more difficult than simply replacing the tissue with a healthy donor tissue. We are working with a number of folks on bionic and biological therapies and replacements for retinal vision loss, but it is a challenging prospect despite what some commercial organizations would have the media believe.
In addition to the above mentioned corrections, there are other problems with this story. In particular, apparently the child was born blind from birth which would suggest that depending upon how old the child is, there will be problems due to vision being occluded during certain critical periods of vision pathway development. This means that there may be no vision in the eye that was clouded anyway, or that vision may not be fully "normal" and likely will never be.
(yes, I am a vision scientist)
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You are not reading the article very carefully. Only the cornea or the transparent outer portion of the eye was transplanted in this case, NOT the whole eye. Furthermore, the two references you report are bad science. First off, let me ask you if organ rejection is something to be considered, would you trade a lifetime of immunosuppresants causing kidney damage and joint disease for vision? Next, the two references in Wired are missing the boat and were written by some very deceptive science. Dobelle is a bit of a crackpot who is using high current electrodes on the surface of the brain and is kindling those patients brains increasing the likelyhood of seizures. Indeed seizures have been reported in those patients. Furthermore, from a conceptual point of view, stimulating visual cortex with crude electrical stimulii will certainly make one see phosphenes, but you can also see them by getting punched in the head. In other words it is not vision and those that are suggesting it is are either deceived or worse. To make things even more dubious, Dobelle has yet to publish his work in a peer reviewed journal and has to perform it outside the US because nobody will let him do it here.
The issue is much more complicated than these individuals would have you believe. There are a couple of corporations that have been started that are very good with media hype. They have good engineers, but the engineers are looking for a solution without understanding what the biology is.
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Making stem cells to specialize into kidney cells is not quite as hard as producing functional neurons and making their growth cones migrate exactly where wanted -- The "wires" aren't the biggest problem, it's the signaling that takes place to connect the wires into something that has a wanted physiological meaning.
And there's very active research going into understanding nerve cell targeting. The problem is just that the successful process of nerve cell growth is a result of a fine balance of a huge number of extracellular signals -- different guidance cues, repelling signals, survival factors, cell-to-cell adherence molecules, etc, etc. The basis is known, but it also appears to be one huge area of intracellular signaling research to cover.
The input really comes from external stimulis, but yes in a way, what we see is the brain's own interpretation of those stimulis.
:
The information is never used as-is by the brain, but at each stage it processed, and information is extracted and spareted.
The vision, for exemple, doesn't work at all like in a computer with a pixel grid.
The input from the cones and the rods (the "pixels") is not sended as-is to the brain. Instead, in other layers of the retina, value from rods close to each other is compared (for : exemple you have "off-/ and on-centers", a signal is genrated only if surrounding cones are off and central cone are on, meaning there's something in the middle of that region).
The information transmited in the optical nerve isn't "pixel at coordinate (150,175) is color rgb(126,129,32)" but "there a change between these points and their neighbours, so there must be something there".
Further stages in the brain works the same way
point are compared together to extract edges (comparing point close together), or motion directions (comparing the timing between two near region).
Then motion, shape, colour, etc... is processed independently in deffirent arrea of the brain.
This analysis is also done at different frequencices : some region compare difference between point very close to eachother, where other regions compare global differences between the two half of your field-of-view.
So : when you see a red pen falling, you're brain isn't processing the images at a whole (not like a sequences of pictures of the pen falling).
But one region of your brain say it found a red object, another region of your brain tells there's an object that is long and thin, a third region see ther's motion going downward, etc...
Also, it isn't possible to have a single nerve fiber for each "pixel" while keeping a high resolution. So there's some kind of information drop : only the center of the view has a high density of receptors (cones & rods), the rest of the field of view has much less receptors.
Only the center of the view can see fine details.
The rest cannot give details, but can still give an alrt if there's something, and you'll automatically point your eyes int that directions to bring the interesting objet in you "high resolution" zone.
The whole scene is the kept reconstucted in some kinf of mental visual scratch pad.
So when you look at a plant you can see it well with all details, leaves, etc...
Then when you look at your computer screen, you can't see that plant that well, but even in your peripheral vision you can still a bullry green spot, and you remembre that you saw a plant there. Even if you can't see details anymore, your brain can still notice that the green spot has suddenly turned brown-orange. You turn your eyes and see that you can is trying to eat your plants....
This also explains why we don't "see" our blind spot. (Due to some poor cabling, the optical nerve is running thru the retina, and there's no receptor in that place, to leave room for the nerve).
It's like a grid with some pixels missing.
The vision works by comparing points. It's just that in the blind spot, the brain is comparing receptors that are VERY far appart. So if something small is located just in the blind spot, we won't see it, but we won't even realise that we are missing it, because when the brain compare the points above, below and on the sides of this spot, it doesn't notice any change, so the brain thinks the background is continuous. (That's what some call 'filling the gaps').
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