Dr Patrick Degenaar, University of Newcastle
We depend on light more than you might realise - our eyes are completely dependent on light to sense the world around us. Without light, we couldn’t experience a beautiful sunset, see the faces of our loved ones, or view the natural marvels of the world. But how do we see? And what happens when this process stops working? Patrick Degenaar works in the groundbreaking field of neuro-prosthetics. These are devices or methods that can substitute motor, sensory or cognitive brain functions that might have been damaged as a result of an injury or a disease. Patrick explained to Chris Smith how these devices might work one day in the future...
Patrick - Fundamentally, light comes from objects. They go through the optics of the eye and get imaged to the back of the eye called the retina. When the light hits the back of the retina, we have some cells called rods and cones which act as photoreceptors. They sense the light. Once they’ve sensed the light then the signal goes through a series of processing. And then finally, the final stage of the eyes is cells called the retinal ganglion cells which project through something called the optic nerve towards the back of the brain. It’s worth noting that the visual cortex, the part of the brain which processes our light that’s at the very back, which is why boxers, when they get punched in the face see stars if you like because that’s the visual cortex pressing against the back of the skull.
Chris - Sounds uncomfortable. So, when someone has a problem with their vision, it could be any part of that pathway which is damaged or breaks down but what are the common reasons why people lose the ability to see?
Patrick - The vast majority of people who lose sight in this planet are because of a condition known as cataracts. And that’s where the lens in the eye basically becomes opaque and can no longer allow light to come through. But in terms of what I'm interested in which is in prosthetics, I'm much more interested in conditions which cause some damage but leave the remaining retina intact. One particular condition is called retinitis pigmentosa which has a prevalence of about 1 in 3,000 people. In this condition, the light sensing cells are destroyed. But this still leaves the rest of the eye intact. If that gives then the possibility that if we can communicate with those remaining cells, you can then communicate with the brain and therefore, restore some kind of visual signal.
Chris - So, because the rods and cones have degenerated or broken down, there's no cell there that can physically collect light and turn it into electrical signals that the retina can work on. But because the rest of the retina does still work, were you able to put new signals in, mimicking those missing rods and cones, you could potentially have a working visual system again.
Patrick - Correct.
Chris - But how might we be able to do what you're aspiring to achieve, Patrick?
Patrick - Well, for many years, people have looked at visual cortical prosthesis. It’s actually dates way back to the 1920s in fact. But in 1992, people working on the retinitis pigmentosa disease discovered that the retinal ganglion cells were still intact. For the last 20 years, various groups around the world have looked at implanting various types of electrodes and using those electrodes to stimulate the remaining cells. They could bring back some flashes of light which when there was sufficient electrodes in place, you could make some kind of very basic type of image.
Chris - Is this working? Do we have devices that are capable of stimulating the right cells in the right place to create a visual image that makes sense?
Patrick - In basic theory, it shouldn’t work at all. But it works to a very simple level, fundamentally mentioned before that the eye is really trying to process the world around us. What the eye does is it splits the signal into on and off pathways. These are kind of positive and negative. Fundamentally, this is about creating contrasts. Now, there's only information if there's a different between the plus and the minus pathways. So, if you stick a big electrode in and stimulate both simultaneously, it shouldn’t actually work at all. It turns out that the off pathway is just a little bit slower than the on pathway. As a result, when you do the stimulus, you get a little bit of contrast. You still get to see something. But it’s relatively weak.
Chris - So just very briefly Patrick, are we in a position where we can actually make devices that can stimulate the right bit of the eye to give people some kind of picture?
Patrick - There are no commercial devices in place which will give a very, very rudimentary vision. But the next generation of devices that are about to come out are based on a new technique called optogenetics. These can basically genetically engineer a new layer in the light eye to be light sensitive. This can then do that separation between on and off pathways much more accurately, much, much more stronger. And this should bring back some kind of vision – well, you'd still be legally blind but it would be significantly better than what is currently available.