Retinal Implant Restores Sight in Retinitis Pigmentosa

26 September 2017

Interview with 

Robert Maclaren, University of Oxford

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Now let’s take a look at what modern science can do for a growing problem worldwide, which is blindness. As more people live for longer into old age, more of them are succumbing to sight problems, often because of disease processes affecting the retina, which is the patchwork of light-sensitive tissue at the back of the eye that converts light waves into brain waves and enables us to see. If this is damaged it cannot repair itself and we suffer sight loss. Speaking with Chris Smith, Oxford University’s Robert MacLaren is working with a prosthetic retina, which is currently in clinical trials...

Robert - We're working with a German engineering firm, Retina Implant, and I should say that the development of the technology is really something that’s been ongoing with Retina Implant for the last ten years. We’ve been working with them over the last five years in clinical trials in Oxford. The purpose of the retina implant is to put at the back of the eye a light sensitive array that is electronic rather than biological.

If I can explain it another way - the light sensing cells known as photoreceptors gradually degenerate in diseases like age-related macular degeneration and retinitis pigmentosa. The electronic retina is light sensitive, a bit like your mobile phone with a digital camera, it senses the images and then it stimulates the retina electronically in place of the photoreceptors.

Chris - The retina has multiple layers and in one place are the photoreceptors - the rods and cones. They send electrical messages to cells further down the retina, which is what makes the optic nerve and sends these messages pinging off to the brain. So, in the diseases that you’re looking at, those rods and cones are gone, but the cells that make the optic nerve and can send messages to the brain, they still survive and you’re putting signals into those cells?

Robert - Yes, that’s absolutely correct. The pathology of retinitis pigmentosa is loss of one layer of the cells - the light sensing cells. Of course, if someone’s lost these cells, they are unable to perceive light at all and they’re completely blind, but the eye itself remains relatively intact. The eye looks normal, it moves around, it focuses the image and, most importantly, the optic nerve which connects the eye to the brain is also relatively normal.

So the technology that we’ve been looking at with the electronic retina is really for patients with retinitis pigmentosa. It wouldn’t, for instance, be suitable for patients who have a disease known as glaucoma in which the nerve is damaged or, indeed, if the eye had been lost through an injury or trauma.

Chris - How big is the device and how do you, as an ophthalmic surgeon, get it inside someone’s eye?

Robert - It’s approximately three and a half by four millimetres in size and that’s the actual light sensing part which has got 1,600 pixels on it. There’s a flat cable as well that connects it to a power supply, and the power supply is located under the skin behind the ear. So there is a cable which goes underneath the skin, across the side of the head under a muscle known as the temporalis muscle to connect it up to the power supply.

We have to slide it under the retina without damaging the retina. We do that by sliding it through a very small slit in the wall of the eye. It is quite fiddly, I have to say; there’s a lot of connections and things, and placement to do, and it takes a long time to do that. But, as ophthalmologists we are quite used to working in small spaces so it’s relatively straightforward in terms of adapting the technology we already have.

Chris - A person who has it implanted and then you switch it on, what is their experience?

Robert - Well, this is quite an amazing time for us all actually, when we get someone who’s been blind for maybe ten or even more years, who has no light perception to then sit there in that room when we activate the device for the first time, usually about three weeks after surgery, enough time for things to heal up. For them it’s a life changing moment and it’s very exciting for us. Everyone in the team gets to know the patients well, and we’re all very anxious until that final switch on takes place and once the patient’s able to see things we know that the whole process has been a success.

Chris - Do they see colour or at the moment are you just seeing spots of white light on a black background?

Robert - Yes, it’s very much black and white. The light sensing cells - photoreceptors - come in three colours effectively, red, green, and blue and they build up a coloured image but that processing we don’t currently have in the implant -  it’s really just on or off. Sort of similar to the very early television pictures, a very grainy black and white image coming and going. It’s certainly nothing that you would describe as normal vision, but it’s enough for these patients to get around and see things and have some independence.

Chris - Can they, for instance, recognise a face?  Because people who have visual decrements say that they really struggle to see people’s faces across the street; they can’t read their favourite book; they can’t watch their favourite television programme. What level of function do they get with this device?

Robert - Well, that’s very interesting because, of course, the human brain is an amazing thing. And whilst patients wouldn’t recognise a face on a still image, for instance looking at a photograph, when the image is moving around they get a lot more information out of it and they can see and recognise people by the way they move. Also, I know some of my patients have described being able to recognise different dogs, for instance. Of course, a lot of blind patients have guide dogs so there are cues there. But the moving image is the most important and that gives them the cues they need to recognise things in more detail than you would think based on the number of pixels.

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