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Although it is tissue-paper thin, the natural retina contains a complex layering of neurons that work together to convert light into electrical nerve signals. Streaming through the pupil, incoming light hits the retina and passes through its outermost layer of transparent ganglions before running into a thicket of more than 100 million rods and cones. These photoreceptors soak up the light, which changes the rate at which they release neurotransmitter packets. The chemicals, in turn, set off a cascade of signaling first in the bipolar cells (which help distinguish between light and dark) and then in the amacrine and ganglion cells. By the time it hits the ganglion layer, the analog light signal has been completely digitized-it is now a series of nerve impulses which the ganglion cells proceed to pump into the optic nerve. The optic nerve’s 1 million fibers carry the signal to the brain’s visual cortex, the place where we experience vision.

Humayun and de Juan weren’t worried about what was happening in the brain. What they needed to know was whether people blinded by a disease like RP retained enough intact retinal circuitry to permit them to get a signal into the optic nerve. To answer the question, they approached the eye bank of the Foundation Fighting Blindness, where they obtained eyes that had been preserved from deceased RP patients so that their cell structure would not deteriorate. Counting the retinal cells at 100-micron intervals, says Humayun, “We found a near-total absence of photoreceptors.” That was as expected. The important discovery was that 30 percent to 80 percent of the other retinal neurons were still intact.

A step in the right direction, but it remained to be seen whether the cells remaining in a blind person’s retina could function. “We had no idea what the effect of 50 or 60 years of degeneration would be on the response of these cells,” says Humayun. There were other unknowns. From animal experiments the team knew how strong an electrical stimulus was needed to elicit a response from the retinal cells, but they had no idea if this signal would produce anything like normal sight. Was it possible that when the current hit the vitreous gel inside the eye, which is 99 percent water, it would simply diffuse out and appear as one huge flash of light? Even if they produced an image, says Humayun, “Would it look like a dot, be blue or green? Would it be something that is appealing, or would the stimulus be so noxious that patients would rather be blind?”

Because these questions could be answered only by a live patient, seven years ago Humayun and de Juan put out the word that they were looking for a volunteer. A colleague put them in touch with Harold Churchey, a former welder who ran a snack bar in Maryland’s Washington County Courthouse after RP blinded him. Churchey was game, even though he would have to remain conscious as the physicians sunk a probe through the wall of his eye, then electrified it. “I might be over the hill, [but] if I can help some young person, I am for it,” says Churchey. Later, his twin brother, Carroll, also blind, would join the experiments.

The first of the team’s 15 human experiments took place at Duke on September 17, 1992. Peering through Churchey’s pupil with a surgical microscope, Humayun pushed a hand-held probe through the white of his eye and back toward the retina. The probe held a single platinum wire, coated with Teflon and embedded in silicone rubber. De Juan and Humayun started applying small electrical pulses of a few hundred milliamps, but for 20 minutes Churchey saw nothing. “You can imagine the level of anxiety as we checked every possible circuit,” said Humayun. When the physicians finally pushed the probe so it nearly touched his retina, Churchey announced that he was seeing…something.

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