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National Library Week Event - Living Well With Low Vision And The Science Of Glaucoma

When: April 15, 2010 at the Downtown Library: Multi-Purpose Room

The loss of vision can be devastating to an individual - and it is one of the most common health care concerns today. Approximately one person in three has some form of vision-reducing eye disease by the age of 65. The most common causes of vision loss among seniors are age-related macular degeneration, glaucoma, cataract and diabetic retinopathy. This event will cover current trends and treatments for individuals with low vision, and what is being discovered through research. Speakers include Lylas G. Mogk, M.D., Henry Ford Health Systems and Sayoko E. Moroi, M.D., Ph.D. Glaucoma, Cataract, and Anterior Segment Disease, Associate Professor, Ophthalmology and Visual Sciences, University of Michigan. There will be ample time for audience questions.This event is made possible through Partners In Research grants R03 NS065493 and R03 NS065491-0 and is co-sponsored by the Michigan Institute for Clinical and Health Research and the UM Health Sciences Libraries. The Ann Arbor District Library is currently the Washtenaw Library for the Blind and Physically Disabled. The event is also being held in conjunction with AADL's upcoming Low Vision Fair at Washtenaw Community College on Wednesday, May 12.For more information on glaucoma take a look at our books on the subject. Articles and current research can be explored in our research databases MEDLINE and Health and Wellness Resource Center.

Transcript

  • [00:00:00.00] CELESTE: Thank you all very much for coming tonight. It's a beautiful, beautiful day outside. So, it's wonderful to see so many people here tonight. There are a couple of things I want to talk about before we get the ball rolling. The Washtenaw Library for the Blind and Physically Disabled came to the Ann Arbor District Library last year in February of '09, and we're absolutely thrilled to be able to provide service for people who have visual or physical disabilities that cause them to not be able to read standard print. We serve people of all ages - from young children to older adults. And if you know of anyone who could use this service in which we provide either braille or audio books to you, free to you, to your home, and then sent back to the library so we can send you more materials; if you are interested in a service like this or know someone who might be interested, please have them give us a call back at the library. The numbers 327-4224. And you don't need to write that down because we have all kinds of different promotional materials outside at the table.
  • [00:01:36.26] The other thing I want to tell you about the library for the blinded physically disabled is it's not just here at this location. If you come to any of our five locations across Ann Arbor or in Pittsfield Township, you can be served by someone at any of the service desks, whether it's the reference desk or the circulation desk. If you have questions any of our staff are happy to answer them for you. The physical collection of materials lives in this building because it takes up 20,000 items; it takes up quite a bit of space. So if you want to physically pick out your own materials you can come here and be taken downstairs and shown the collection. But if you'd like to call us on the phone or email us and be served via the mail to your home, you can do that at any time that you want. So, please let us know if you're interested. Our goal is to serve everyone who qualifies in the county and that's potentially up to about 5,000 people.
  • [00:02:25.11] So, let's get the ball rolling and get people sign up for service. One way to find out about services available to you, not only from the library, but from vendors who have products that might be of interest, is to come to the Washtenaw Community college - the William Moore Center - on May 12th, which is a Wednesday next month, and we're going to have a vendor fair and special events happening on the hours. So visions-- you might have seen a big bulletin board as you walked in the library and if you couldn't have seen it but you read braille--we have flyers out about it in braille and in large print. So let us know if you're interested in learning more about that vision vendors fair as well.
  • [00:03:04.73] Specifically to the program tonight, I want to thank our partners at the University of Michigan. We are in a happy relationship at the University of Michigan of having received a National Institutes of Health grant, to get the public involved in clinical research and raising awareness of clinical research topics; how it might involve you and your lives, how clinical research affects your lives, and how you can become involved in the process. So, we work with Ms. Shah, and I'm going to introduce Doreen in a moment to tell you about her speakers. And we work with the Taubman Health Sciences Libraries to bring you these programs to learn more about particular health topics and clinical research opportunities that may be of interest to you.
  • [00:03:46.18] DOREEN SHAW: Thank you very much Celeste and welcome everyone this evening. As Celeste was mentioning Celeste and I are the co directors of a grant from the NIH that allows us to bring these topics to all of you, and were thrilled tonight to bring a topic focused on low vision and glaucoma. This is the first time we've done this particular topic and we have been delighted to have both the University of Michigan and Henry Ford Health System partner together in providing us wonderful speakers.
  • [00:04:20.64] Our first speaker this evening is Seiko Moret and Dr. Moret has her medical degree as well as a PhD in pathology. She's an associate professor of Ophthalmology and Visual Sciences at the University of Michigan Kellogg Eye Center, and have special interest in glaucoma, inherited glaucomas, clinical trials, complimentary and alternative medicine, and medical compliant.
  • [00:04:45.60] Our second speaker is Dr. Lilas Moke. Dr. Moke has a medical degree as well, and she is an ophthalmologist and medical director of the Henry Ford Visual Rehabilitation Centers. She's also chair of the American Academy of Ophthalmology Vision Rehabilitation Committee and the SmartSight Initiative in Vision Rehabilitation. She also chairs the Michigan network for Vision Rehabilitation for seniors.
  • [00:05:12.03] So, you can see we have brought the best that medicine can provide to talk about that's very important topic to you this evening. As you were told at the very beginning, because this is a grant, we actually collect data about your impression of the evening and what you've learn from it. So it's important to us at the end of the evening for us to collect up those blue forms from you, so thank you very much for doing that. I'm going to have our speakers give their presentations and then when we conclude, the screens are going to go up there, there's a table there, and they're going to take your questions. So please, if you have questions, hold them for end, and we'll be delighted to run the microphone around to you at that time.
  • [00:05:51.82] DR. SEIKO MORET: I want to make sure to let you all know, and maybe many of you do know, that we have just opened our brand new Kellogg Eye Centered tower, the partner tower. We started seeing patients there March 1st and it's a beautiful facility there. So my disclosure is just to let you know that I do have a clinical research grant from Merck, which is the pharmaceutical company which doesn't provide some glaucoma medications. And I've just completed a 6th edition of the Shields' Textbook of Glaucoma, and that royalties from Lippincott.
  • [00:06:25.59] So, I want to share with you currently a 7 year old boy. He was born in August 2002. His medical history is such that he had premature fusion of the skull bones, meaning the skull bones - rather than as you know an infant has soft spots - his fused together, and that's a problem in relation to a development in growth bones. So, he had some major neurosurgery early on. But as you can see he has very small eyes and these little white dots here are actually cataracts; he was born with cataracts. This little child had over 11 surgical procedures, 30 examinations under general anesthesia, and I know it's hard to appreciate but Dr. stephen Archer was initially involved with this child, this boy, taking pictures of his optic nerves, which I'll show you a little bit more with the anatomy.
  • [00:07:19.91] And then this is later on. Greg Dukes became involved too as our ocularist. That's the person who specializes in how to make artificial eyes. These are artificial eyes, but he made thin essentially plexy glass shells so that this little boys orbits could grow. The eyes actually grow up till about age six to eight years old. But if you're born with a very small eyes, then the bones won't grow properly. So he had to be fitted with these clear--you can probably appreciate it's really shiny sort of here, all over the surface--with these little shells on his eyes.
  • [00:08:00.52] And that's him when he was probably about nine months old, after Dr. Archer got him fitted with glasses, after having cataract surgery. Well I became involved later on because he developed glaucoma. And in children who end up having cataract surgery, because they're born with cataracts, it's probably anywhere from 30 to 60% end up getting glaucoma, and it's a big challenge on how to manage these. This little boy is now seven years old. I actually talked to mom. She's let be present is case before, but I wanted to make sure to get her permission that it was OK in front of this venue, and she said that was fine. His pressures where high in the 50's, and just to let you know, normal pressure range 10 to 10. So his eyes were almost as hard as marbles; they were rock hard.
  • [00:08:48.54] I had done multiple glaucoma surgeries on him, had medical treatment on him; his eyes are smaller than normal, so I'm very nervous about doing any conventional type of glaucoma surgery on him. And now has pressures vary between the high teens low 20's - in that range. He's one of the smartest children in his class, he has mainstreamed to the public school education, he's fluent in braille, and his mom just told me today that he's eligible for national competition in braille reading. So, he maybe going soon that national competition. But this is the type of situation when I look to my colleagues, other glaucoma specialists' help. This child is going to need a lifetime of care and can we try our best to give him a lifetime the vision; that's our challenge.
  • [00:09:36.93] So, our overview tonight--I want to introduce you to the field of epidemiology of glaucoma and vision problem--to provide you information about anatomy, what I would call 101 of the eye, to inform you about glaucoma - the pathology treatment, genetics, and future eyecare. And then Dr. Moke will be talking also about her area of expertise in relation to how we manage low vision. The part one - What is epidemiology? I actually directly copied and pasted this from Wikipedia, and I will show you some more later; I didn't want to overwhelm you. But essentially, epidemiology it's looking at different factors that affect both health and illness in different populations, and it's really the underlying pennings of how we decide to treat a patients, and try to make sure to have preventive medicine to sustain health. Now, this is the rest of the definition, and I know it's a lot, but the key things I want to show you is that you probably heard the words evidence-based medicine. This is where we want to make sure that there is solid science behind how we treat you and how we treat ourselves. It has to do with both communicable and noncommunicable diseases. Looking at, for example, infection, there's been a lot of obviously discussion - H1N1, those kind of things. Of course the CDC's involved, and many people are involved, and those are issues with communicable diseases. But then there are also some diseases that are not contagious.
  • [00:11:13.63] There's important research that needs to be done related to study design, how we collected data, how we analyze the data, and then part of that is how we design studies looking that models once we get the data. And when we do this research we have to have an idea; that idea is called a hypothesis. And we have to take a scientific approach to make sure we are doing the study properly. We'd like to then share our findings with the public and that's what we do, it's called peer review publication. That's sort of the standard that academics have in all fields of study--not just medicine--all fields of study. The areas that we look at are in relationship biology, we look at statistics, and then what's called geographic information science or GIS, where we look at how we store data and map disease patterns, because we want to look at this is the global issue. And then also social sciences--Not only is there genetics, infectious diseases, communicable diseases, noncommunicable diseases--but how does our own health, behavior, diet, exercise; how does that impact disease. So what's the global burden a visual impairment? Well in a view article by the Dedonas and the BMC medicine; this with 2006. It says to me that there about 260 million with it visual impairment. About 120 million art actually really disabled because they don't have glasses just to fix their refractor vary, meaning just glasses for distance for reading. 42 million are blind in one eye and then specifically for glaucoma, Dr. Quigley and Dr. Broman have estimated worldwide statistics in relation to 2010 and 2020. In 2010 they project this year that they're about 60.5 million people with what's called open-angle glaucoma and angle-closure glaucoma, and I'll go over those definitions in a cartoon when I show you the anatomy. About 3/4 have what's called the open-angle form of glaucoma. Women comprised a little bit over half of the open-angles, about 70% of the narrow former angle-closure glaucoma, and almost 60% of all forms of glaucoma; so women seem to be affected a little bit more. Asians represent nearly 50% of those with glaucoma, and about 90% of those have what's called the angle-closure form a glaucoma. Blindness and both sides, that's bilateral blindness, it's present in about 4.5 million people with open-angle and about 4 million with angle-closure. And they're projecting in 2020 that nearly 80 million will have either open-angle or angle-closure forms of glaucoma; so, it is the public health issue.
  • [00:14:16.46] Now what about in the US and in then Michigan? I've listed here all these studies here, and this can be found at the National Eye Institute, National Institutes of Health, looking at some eye date and tables, where they present this information. I've just really synopsized it. You'll see ginormous Excel of piles have helped this, so I synthesized it here. So over the age of 40, if you look in the US, there's about a million and again, you can see that it disproportionately affects women compared to men. You're looking at low vision here - 2.4 million by 2020. It's projected to almost double - about 4 million projected. Macular degeneration--you can see here's 1.6 million, cataracts - 20 million. The nice thing about cataracts, however, is that's fixable; you can have surgery for that. Diabetic retinopathy--with the concern right now in relation to obesity and the epidemic--this is a very big concern, because 5 million affected over the age of 18, and that is projected to really increased. Open-angle glaucoma it's about 2 million, and among those who are blind in both eyes - oh you mean both eyes - it's about a 100 thousand. And then overall blindness, over the age of 40 by 2020, is expected to be about 1.6 million. In the State of Michigan--I don't want to be too much in the numbers, so I actually counted and saw where Michigan landed in relation to all of the 50 states--unfortunately we're on the top 10 for all of these issues.
  • [00:15:54.58] So, as healthcare providers we really have our work cut out for us. So, this is a typical question I put out - usually to physicians and residents in training - I ask, "What's your estimate of under-diagnose glaucoma, meaning people everyday walking around who don't know they have it?" 50%. More than that. And here's the studies that show that. So there are what are called large population studies where they looked at in the U.S. that they suggest that over half of glaucoma has not been diagnosed. In Baltimore, in the Baltimore eye survey, it was nearly 60%. Out in the Southwest, the corrective vision eye research study - 62%. Many of these individuals, when they're screened and looked at, have already suffered severe visual field lost, and all explain a little bit of that later on in the anatomy, before they're even diagnosed. And that's the trouble, most forms the glaucoma, your eyes don't hurt. There're no symptoms until it's very late stage. So, how often do individuals with untreated glaucoma go blind? About 50%. And here are the study's. For some patients, the failure to diagnose the glaucoma or effectively treat it--and I'll just mention a little bit about that--which can lead to rapid vision lost.
  • [00:17:20.34] Looking in the West Indies , they looked at the natural history of glaucoma because many of the patients there they didn't have the eyecare, couldn't afford the medications, and surgeries are very challenging to manage with the follow-up. And in 205 patients, or people who are suspected of glaucoma in Saint Lucia, 16% got blind in the least one eye over 10 years. And this is a certain NIH study that was used to determine blindness, almost 10% went blind in both eyes.
  • [00:17:57.26] The other thing I can mention to that if you're interested, I can provide this slides set to you because I know there's information if you want to look it up later. More than 50% percent of those eyes that progressed to end-stage glaucoma, essentially had pretty healthy vision. The other important point to learn is that this lack of effective treatment can result in blindness. So, Olmsted County Minnesota--this is in the area of Mayo Clinic, right? Very good reputation, people have access to healthcare, primarily caucasian individuals, don't think of too much there about some socio and economic status situation; they have access to healthcare. They estimated there that the probability of blindness after 20 for people who had established diagnosis the glaucoma, 30% percent in one eye; even higher there; 10% percent in both eyes. For people who had high eye pressures, it's called ocular hypertension, 114 of those patients were identified in this data set, in over 20 years almost 15% where blind in one eye, 4% in both eyes.
  • [00:19:10.99] So, conclusions about this, glaucoma certainly a leading cause of blindness in African-Americans; I didn't go over that data. Glaucoma the second leading cause of blindness worldwide; that was from those reviews that I've mentioned. It disproportionately affects women and Asias, and the and question is why? Why? Part 2, I want to go over some anatomy of the eye. This is an anatomy schematic cross-section of the eye here. And as a glaucoma specialist, when I examine a patient, I look at what's called the anterior segment; that's this part of the eye here. Anterior means front. I look at the eyelid. I look at the skin of the eye call conjunctiva. I look at the cornea, the clear window here. I look at the front chambers. I look at the color part of the eye called the iris, and I look at the lens right here; that's called the anterior segment. Those are all important things for me to assess different forms of glaucoma, when I do my exam, and also if I'm thinking about surgery, what approach I should take. Aqueous Humor Dynamics - aqueous means liquid and humor means liquid also, dynamics means how it moves, and that determines the pressure. So the fluid is made by this gland called a ciliary body, right here, that suspends the lens. It goes out the drain right here, and I'll show a little cartoon differently, and then out of these other tissues. But these are also tissues that I'm concerned about when I think about surgery or how we want to treat somebody with medication. Then, when I look inside the eye in the very back here, I want to look at possibly end-organ damage or how I want to prevent that. I look at the retina, which is this part of the back the eye. I want to look at the optic nerve, which is right here, and then more details, which you can see in some other pictures, actually. I want to look at how healthy that tissue is. So, in general when we talk about vision, basically explain to my patience that light comes in both sets of eyes, they travel in these cable tracks to the optic nerves, part of the vision crosses to both sides, and then they eventually come to the back of the brain here called the visual cortex. And this is what we call the visual pathway. There's the very specific pattern on how the nerve fibers go back to the back portion of the brain, and the way we assess that is number one, division, but then number two, we also look at what are called visual field. And that's a test where a patient puts their head in what looks like it big like goldfish bowl, we test one eye at a time, and when the lights are presented and then individual see them, you push a buzzer; it's like a video game. So, this is the clinical situation where there's an African-American gentleman, there's no family history of glaucoma, the pressures are in the high - normal range of 23 to 20 - I said normal pressure varies usually from 10 to 21, and is without medications. When we checked the eye pressure or interocular pressure in the office, we only get one time point. But if there's someone I'm suspicious about whose varying a lot, what I do is I have them come in every two hours during our office hours. And this gentleman's pressures varied from 16 to 25 in the right side and 15 to 20 in the left. The drainage angle, which I'll go over with you, are open, so this person would have what we would called an open form of glaucoma. And we'll look at other risk factors in relation to the cornea, and then the visual field is fortunate for this gentleman; they were quite full.
  • [00:23:04.01] But the question I often pose is - What is glaucoma? Well here's where we come to glaucoma definitions. Before the 1980s, our definitions where it was elevated eye pressure. If you had high eye pressures that equal glaucoma. Between the 1980s and the mid 1990s, it became well you have elevated eye pressures and a field defect medical glaucoma. But now we know that it's a little more complex than that. So, we define it as a chronic progressive optic neuropathy meaning it's slowly progressive nerve damage. And it's associated with a particular, what we call, pattern of optic atrophy - optic meaning the nerve and atrophy meaning lost of tissue where it looks excavated back here; where it looks dipped back, which means thinning of the rim of tissue - this orange part here, right here. You get a related loss of nerve fibers and the cells called retinal ganglion cells. It can be associated with high eye pressures, but not all the time. But this is at the present time the only modifiable risk factor that we have to treat glaucoma. As far as other risk factors that we've learned from clinical trials, is that a thin cornea is associated with glaucoma risk.
  • [00:24:29.20] So, why do we performed the visual field? Well as I mentioned, this is an important way for us to assess the function of your optic nerve. And so this provides important supplementary information about vision and also vision loss. Because sometimes it certainly very pathological - meaning there's two disease. There are some people that it's functional - meaning there faking and we can figure that out. Visual fields also we can quantify the defect to look for progression. Other things is that this is typically slowly progressive. But it allows us to determine if there's a change over time and if there is, we have to modify or treatment. So, as I mentioned, the retina at the back of the eye, this is the magnified view of the retina, there is a high order of cellular pathways and the different nervous tissue layers. And what we're seeing is when the light comes through and stimulates these outer cells called the photoreceptors. It sends signals to the brain by these nerve fibers layers. And the way it's pointing the lights, when you put your head in that bowl and we flash the lights, it's only stimulating a certain part of your retina and going to a certain part of the brain, so we can figure out what part is damaged.
  • [00:25:53.24] The history of perimetry this century BC, Hippocrates actually described the earliest vision field defects related to strokes in the brain. Leonardo da Vinci - This is a picture from one of the old history ophthalmic books that actually recognized the extent of what we call the temporal visuals that's out here. And then later on modern perimetry was based on this kind of what we call tangent screen where the patient's side and this side look through this little cylinder tube, and then little lights were flashed up here, and then the person who tested it would then go ahead and mark where they saw the lights and where they didn't see the lights. So, open-angle glaucoma - Open angle-glaucoma, this is about this quarter part of the front part of the eye. I told you this is the lens, this is the back of the eye, this is that gland, that ciliary body that makes fluid. These yellow area show you where fluid is made. It circulate around the lens, through the pupil here, in the front chamber here, and out over to the mesh work; this is this area here through Schlemm's canal. A minor part also goes out to the uveal-sclera pathway. And what I wrote here is actually where our different glaucoma drugs work at. Some work at the trabecular ouflow, some work at the uveal-sclera outflow, and some work this way, in the inflow. And so I usually explain that pressure is sort of like simplified plumbing; there's a faucet that makes fluid and there's two drain pathways - there's this drain and there's this drain.
  • [00:27:32.73] And so we have to figure out which medicines will maximally lower the pressure, either by turning down the faucet or increasing the drained. And if those don't work then we use other approaches. So when I have to diagnose it I have to think about, for example, is it developmental, is it a child, or is it after surgery in a child, is there difficulty in the development to the front of the eye that has anL abnormal-type drain or outflow, or is there retinopathy prematurity. That's called ROP where the front of the eye does not develope normally. Then the more common forms an adults - this is what's called the open-angle form. That's where the drainage angle is definitely open. If you draw a line here just remember your geometry in the cornea, and draw a line here to the iris; that angle I'd say is opened about 35 to 45 degrees there; that's open-angle. But is there something blocking it that we can't see or is there something further out that we can't see blocking it? But that's called open-angle form of glaucoma. Closed-angle form of glaucoma is the difference you see is this iris here. The color part is bunched up and clogging access to the drain. So fluid really built up here, it can't go to the pupils here, and this is where people come in to see us. Because this can happen suddenly, the pressure skyrockets, the patient has the red eye, it's painful. Sometimes they even feel sick to their stomach. And this is usually coming in to us as an emergency as an angle-closure glaucoma. And for any of you who have looked actually at a cold remedy like Sudafed, any of those cold remedy preparations, they will have warnings there to say if you have glaucoma or narrow angles, do not take this. Sometimes those actually change the anatomy of the iris to actually create an attack of angle-closure glaucoma.
  • [00:29:31.55] We get those calls to our office all the time - is it ok for me to take this medication; for the majority of people I say yes. So what is damage to the optic nerve? Well it's a delicate balance here on the see-saw. We want to enhance self-survival before the individual nerves themselves get sick. They start getting really sick and generate and they die. And there's a process of what's called necrosis - if you're in to CSI or those kind of shows here - where we call it a homicide-type of damage where the cells can explode. There's no production of anything. There's a lot of irritation or inflammation in the area, and there can be some breaks in the DNA material. That's what we call a necrosis pattern or cell death. However, in glaucoma it seems to be this kind of almost programmed-type problem of what we call apoptosis. Sometimes we call it a suicide path where its the failure of survival mechanism; we don't understand why. The enhancement of death signals are happening. There's a particular type of pattern in the cells that we see under a microscope with condensation and budding the cells. There's actually very active production of some nuclear material as well as protein products. Usually there's no inflammation. And then characteristically, the DNA tends to break into these size fragments here. And we're trying to figure out why, and can we arrest that somewhere here, that we can shift then the see-saw this way, and tip it back over here; that's the research that's going on.
  • [00:31:16.69] So, clinically this is what tends to happen is that there is the very gradual decrease here in the peripheral vision. People may not notice it because it doesn't take your central vision away. It's the periphery, and then all of a sudden maybe the cabinets stuck out and you didn't see it - bang - you know you hit the side of your head; there's a cut. I've seen some patients come in to us with that type of problem and history.
  • [00:31:43.60] So we have many many effective medications - you can see here. There's many different types. So, sort of in conclusion, what do we know about glaucoma? Well we want to maintain everybody at 20/20, we want to have minimal impact in vision lost. These here, the pictures of the optic nerve, you can see serially getting worse where it's very pale here, because the nerve tissue is getting damaged and lost. And then going serially from this field to this field, you can see it's getting dark, and that's what happens in glaucoma, and we want to minimize blindness. The risk factors we know from clinical trials, from epidemiology studies, is that older age, higher eye pressure, a thin cornea; these type of factors here lead to glaucoma, and that's how we individually tailored treatment. The risk factors from other studies what we call smaller series, case series, or if there's great value in clinical experience also. We know that there's the family history, if somebody's had some other stroke issues, these other sort of medical issues; that can also lead to it.
  • [00:32:53.77] But here's where you want to see the big picture in different areas of medicine. We need to understand how the areas of cell biology, neuroscience, genomics, genetics; all these fields of medicine, which I feel fall into biological networks, affects this pathway. Then we also want to know how the environment, the area social sciences, and this comes from all these different areas of studies - clinical trials, nutrition, microbiology - impacts us. Genetics wise, I just want to let you know where a big research push is being pushed. We have approximately 70 know genes or areas on the chromosome where we know there are glaucoma locations. But that only accounts for under 10% of the glaucoma. The ones that I've listed here and blue are the ones that we've been involved with at University of Michigan, so we've done quite a bit of research on that. And if you look at the human chromosome map here, what I did is I marked up here or what areas of the different chromosomes where glaucoma localizatoin has been. And given this complexity and all the different diseases, so that the mantra that genetics use that this is genetic heterogeneity meaning there's many many genes involved.
  • [00:34:20.13] One of the areas that I'm particularly interested is, I mentioned to you before, that our glaucoma drugs either work to decrease the food production at the faucet or to increase the drain. But how do we choose which medicine to start with? Right now it seems to be more trial and error and I've experienced that myself. When people are treating me we'll see if this medication works, come back and we'll see if it works. If it doesn't work we stop it and try something else. Well, I feel that if we can use the power of genetics we might be able to assess by conventional pharmacology. We know how drugs get absorbed into the I, where it goes into the eye, how it's broken down and eliminated. We also know there's a lot of science behind how they work, how they get to their target, do they - as I mentioned - decrease the food production or enhance the drain. And then typically, yes, we assess how good does the drug work. Is it efficacious or are there problems; is there toxicity side effects. But we know there a genes associated with these pathways and we know there are variations and those genes.
  • [00:35:32.94] The other issue is how does the environment potentially interact with all this pathway here. Well, first you have to make sure someone's taking their medication. But are there other cold medications someone's taking, diet, exercise, that impact the outcome. And this is the area of pharmacogenomics, and my hope is that if we have this type of science, everybody will have some kind of genetic profile and it will let us know, oh, we know you'll respond well to this medicine but not this one, so you shouldn't even been trying this one. And there are fields in medicine, for example in breast cancer research - primarily in oncology - that there are genetic tests mandated before starting treatment, because some of the medicines work if you have this kind of gene change, they don't work if you don't have it. And before embarking on these very expensive medical therapies like Herceptin, which cost over $30,000 dollars a year. You'd wanto to know well sure that it's going to work in you. Personal genotyping - I still call it - I would call it boutique industry right now, but they're here.
  • [00:36:41.71] Our neighbors, Google, partnering with 23 Aimee. They have this on their website right now. They state that there is the markers for how to respond to what's called beta blockers. That's primarily used for heart and high blood pressure, but we have similar medications to treat glaucoma. So, from the genomics, proteomics, these types of all these omics - two-molecular medicine. If we're going to develop a test, what do we want do we want? Well first, we want it to be sensitive an accurate. I'd want those tests that we're getting to find individuals who are at risk that we need to monitor. I want to have genes that would let me know approximate is it going to be an early age onset? Is it going to be a severe-type marker? And it's going to be rapid progression? Because what I want to do is find those patients who are going to have a rapid course that I can't intervene and prevent blindness; that's what I want. I want to look for markers for treatment response, for example what I gave you with the breast cancer. We want to find markers that help us determine who would respond best to certain medications, and also to avoid toxicity or side effects. Then this will allow us to target or customize treatment for the patient, based on their profile. The public health impact that would change the natural history of disease with earlier diagnosis. This'll be with the personalized treatment for medicine based on our genes, on our proteins, and environmental risk factors so we can improve the outcome. And in the long term, I modified this.
  • [00:38:24.76] The former director of NIH was Dr. [? Zhu Huni ?] but at our National Vision Eye Research meeting, one of the things to put in perspective, if you look at age over time here - this is the child at birth and obviously living pushing to 75, 100 years old - if an infant has glaucoma, no treatment, they were uniformly go blind. There's no question, it's a surgical diesease. But hopefully we can have successful surgery, and over a lifetime have only minimal or moderate vision impairment to keep that child seeing for the rest of his or her life. For age-related glaucoma or, for example, macular degeneration, usually everybody starts at 20/20, but then there's the gradual decline in vision. What we want to do with chronic diseases like macular degeneration like glaucoma is have our treatments push it out here so we delay the drop in vision and prevent somebody from going blind. And so what we've done in glaucomas, we know from our clinical trials that lowering high pressure slows glaucoma progression. Your tax dollars were at work there. We've had success in finding the rare forms of glaucoma. And what we night need to do now is find those genes for the common forms of glaucoma. It's called NEIGHBOR and we are a partner in that, with multiple different centers.
  • [00:39:51.13] My area of research is in pharmacogenomics, and we want to understand some basic pathways involved in glaucoma. We're doing that at Michigan also. And all of these then will work toward potentially new treatments for protecting the optic nerve and potentially even stem cells. Now I'll turn the talk over.
  • [00:40:17.00] DR. LILAS MOKE: I'm actually going to talk a little bit about minimizing risks of vision loss and then about living fully with vision loss. But first I'd like to ask, how many here have glaucoma? And how many have macular degeneration? How many have vision lost from any other cause? OK, now, as Dr. Moret said, for glaucoma, early diagnosis is absolutely critical, and compliance with treatment is absolutely critical because there aren't any symptoms until it's too late; until it's already far advanced. Macular degeneration is different in that regard. First of all, the symptoms come immediately, almost, but since there are no real treatments to prevent vision loss - certainly not in dry macular generation, which is 90% of it - but also for many with wet macular degeneration. It's very important to take steps to minimize your risk before a diagnosis. So rather, if you are checked regularly for glaucoma in that checkup, macular degeneration will be found as well. But the real reason for having regular checkups is to find glaucoma, and macular degeneration you should do something [INAUDIBLE] before it happens.
  • [00:41:43.63] So, in line with the approach to what research it does for us, how do we know what to tell you what to do beforehand? So, as Dr. Moret said, when a cause is unknown then everyone - all of the clinical researchers, the clinicians, the biologist, the geneticist, pharmacologists, the biochemist - all collect information, put it together, and try to figure out what's the pathology and therefore, what's their risk factors. So, with respect to macular degeneration, which I'll address, smokers where observe to have more macular degeneration than anybody else. So, what smoking does he is produces free radicals, it undermines antioxidants, it decreases Vitamin C absorption, and it promotes inflammation. So any or all of those could be playing a role in macular degeneration. Of course, non smokers also get macular degeneration, but they are exposed to secondary smoke, and many of the toxic substances in smoke are also in other places in our environment - in airL and water in industrialized countries. Also it's older individuals who development macular degeneration, and aging is also associated with production of free radicals. So we have two sources now - smoking and aging - that they give us more than the normal amount of free radicals. In addition, Caucasians were observe to have more macular degeneration than other people. And Caucasians, who have less melanin in the visible parts of their body also have less in the layer under their retina that protects the retina and the macula from sun. So, now we have age, smoke, and sun as sources of extra free radicals, in the populations that were found to be at highest risk. Since free radicals have to be neutralize by antioxidants and antioxidants have to come from food, the first nutritional research on macular degeneration was focused on antioxidants.
  • [00:43:52.42] Many smaller studies proceeded it, but the age-related macular degeneration study known as AREDS was the definitive study which followed over 3,000 participants over an average of six and a half years, in a perspective, randomized, double-masked controlled study. That means that some of the people in the study were given a combination of vitamins and some were given a placebo, and neither the people taking the vitamins nor the physician's giving them knew which was which. Which brings to mind in this wonderful cartoon in which this forlorn looking gentleman says, "I believe that in life we're divided into two groups. Now my life is ok, but I think my group got the placebo." Now the AREDS found that the combination of supplements actually did slow the progression of macular degeneration in about 28% of the people who had either moderate macular degeneration or advanced in one eye. And that combination is 500 mg of C, 400 of E, 25 IU of beta carotene, and 80 mg of the zinc plus 2 mg of copper just so you don't get a copper deficiency with high zinc intake. The AREDS formula is therefore recommended for patients with moderate or severe AMD, and many opthalmologists recommend it for anyone with even early AMD. The AREDS formula for smokers is without the beta carotene.
  • [00:45:21.42] Now with respect to sun, lutein, which you probably have all heard of at this point, and zeaxathin protect leaves from sun damage, so the question was whether they also protect the macula in a number of studies follow. One found that those who ate five servings or more a week of dark green leafy vegetables, had significantly less macular dgeneration. Others show that eating lutein increase blood levels and that in fact in a twin study, it was the eating of the lutein and not genetics that produced the high blood levels. Others showed that more lutein in the blood meant more macula pigment, which is protective, and one studies show that more lutein increased macular pigment and increased acuity and contrast sensitivity. And to answer the question or address the question of whether the sun really does contribute to macular degeneration, Japanese quails were used because amazingly they have maculas similar to ours. They were subjected to blue light, and it was found that those who were given lutein and zeaxanthan before the light was shine them for a number of hours, did not sustain the damage that the birds who didn't have lutein and zeaxanthan did. And it turns out that the Chinese have actually known this for centuries because they have been eating little tart berries, which translated as wolfberry for their eyes for centuries. Now because of all this evidence a second definitive AREDS study is going on right now, and they had added to it the lutein and omega-3 fatty acids, which we'll talk about in a minute. Now any injury in the body triggers an inflammation, an inflammatory response and that happens in the macula as well, but rather than having the effective healing, it actually causes further damage. The recognition of inflammation as a factor in macula degeneration was enhanced by genetics studies, which is identified a gene variant as more common in people with macula degeneration, and that gene controls inflammatory response.
  • [00:47:36.42] Another study found that those taking nonsteroidal antiinflammatory for arthritis had only 1/10 of the macula degeneration as an age match population. And with respect to macula degeneration genetics, I should add that University of Michigan just announced this week identification of another gene that affects cholesterol metabolism that is associated with macula degeneration. So, genes play a role in inflammation, but more people have macula degeneration than have that gene variant. So the plot thickens when we look at food which we all eat. A number have studies have shown that high intake of omega-3 fatty acids is associated with less macula degeneration and a high intake of omega-6 fatty acids is associate with more macula degeneration. Omega-3 and omega-6 are essential fatty acids which means that we have to eat them, we don't produce them.
  • [00:48:37.06] So let's look at each one of these. Omega-6 comes principally from corn oil which is our biggest crop in the USA and other light vegetable oils, and from animals that have consumed those plants. Omega-6 produces arachidonic acid and arachidonic acid produces series 1 and 2 prostaglandins. Prostaglandins help regulate the cells' activities and series 2 prostaglandins promote inflammation at which we need in response to injury or stress. OK, that's omega-6's. Omega-3 comes from flax oil, nuts, and green vegetables, and it produces DHA and EPA. EPA and DHA both also come directly from fish liver oil and fish eggs. DHA is a component of plasma membranes of the rods and cones in our retinas, and EPA produces series 2 prostaglandins, and they modulate inflammation. So, the 6's promote inflammation, the 3's modulate it. We need both of these; we need to start inflammation and we need to stop inflammation. But these two fatty acids - the omega-6 on the left, and that's the arrows down just show the reaction to get to that endpoint prostaglandins. And omega-3 on the right use some of the same enzymes to get where they're going. The enzymes are the green ones in the middle and they worked on both chains. So, that means that we need to eat an appropriate ratio of omega-6 and omega-3 so they each get a shot at their share of the enzyme.
  • [00:50:20.52] And that's where things go awry, particularly in the USA. In the last several decades we have introduced large quantities of omega-6 oils into our food supply from soy, corn, cotton seeds, and safflower for two reasons. First they're used to make artificial fat, and second they are used in processing and packaging of virtually every food that comes in a package. When this study was published, showing association between the omega-6 fatty acids from vegetable oils and increase macula degeneration. One of our occupational therapist and I went to a large convenience store and looked at every food item in the store, and we only found four things that did not have vegetable oil on their label, and those four things were mustard, ketchup, relish, and pistachio nuts. Everything else had all of the a snack foods, the health food bars, the cereal, the frozen food, the canned food, the ice-cream, micro-wave popcorn...everything has it in it. So our ratio of omega-6 to omega-3 is likely to be as scued. Now estimates that I've seen of the optimum ratio is 4:1; we should have four times as many omega-6's as omega-3's.
  • [00:51:43.13] But it is also estimated that the average American diet gives us in the neighborhood of 20:1, so we're getting five times more omeag-6's without even realizing it just because we're eating food out of a package. So, for broad steps, and it's much much more complicated than this, but just the big broad steps are handy. We have aging and environmental exposures causing excess free radicals, which injure the macula, which in turn trigger an inflammatory response, which causes further damage, and then this blocks the flow of nutrients in and waste materials out, and it finally results in the two forms of macula degeneration.
  • [00:52:22.92] So, given what we understand now, to minimize your risk of developing macula degeneration and to retard it's rate of progress if you already have it, here are the do's and don'ts. First, decrease your exposure to free radicals by not smoking and avoiding secondhand smoke, and by wearing sunglasses--preferably those that block the blue wavelengths which in commercial lenses are generally in the family of yellow, orange, amber, brown color lenses. Second, increase your antioxidant intake by eating a lot of dark green leafy vegetables. Third, decrease inflammation by eating a lot of omega-3 three fatty acids and fish and fish oil, flax seed, and nuts. And eat as little packaged food as you can. And forth, optimize your circulation with exercise and blood pressure control.
  • [00:53:15.78] Now the underlying message is that a good diet is most likely helpful for everything. But another question is can we actually get the nutrients we need from food if we do everything right? Now nobody knows that for sure, but I think there are some persuasive arguments that we may not be able to. First, we're all getting a very heavy load a free radicals from the environment, which means that we need extra antioxidants to counteract them. Secondly, it's unlikely that the people getting macula degeneration are abusing their diets because if they were, they would have died of a stroke her heart attack before they got old enough to get macula degeneration. So, they tend to be the healthy ones who are still around at 85, 90, and 95. It's more likely that they are making relatively good food choices, but not getting enough antioxidant nutrients from their food to protect the maculas from the [? aphids ?] free radicals.
  • [00:54:11.07] So, we don't know the extent of the impact. The nutrient content of our food, from industrial food production additives, packaging, in addition to the industrial chemicals in the soil, and the lag time between picking and eating our food--but it is likely, given all that--that our food doesn't have the nutrient content that our grandparents who did, just at a time when we need more of it, because we have more free radical exposure. So, food selection is important, but food production from growing, to processing, to packaging, to distribution, is also important. And to the degree that any of us can support high quality food production, it is in our best interests to do so.
  • [00:54:56.90] Now with regard to supplements, no one knows whether they are necessary or helpful for those at risk for AMD, but certainly those with AMD should be taking the AREDS formula. If you do not have AMD and wish to take vitamins, then just a good general multiple vitamin would be advisable, not the AREDS formula because it has a very large amount of zinc in it. Now the reason we treat eye diseases and the reason for all of us to reduce the risk for eye disease is to save our vision. But what if you are among the millions who are beginning to lose vision or have already lost some vision from macula degeneration or glaucoma or any other cause.
  • [00:55:43.65] How do you deal with losing vision when your entire life structured with sight. If you're like most, you get angry. When Grace was abruptly told to stop driving, this sweet 82 year old grandma said, "I dreamed of running over my ophthalmologist andin my new gey Lincoln."
  • [00:56:01.71] [LAUGHTER]
  • [00:56:03.55] DR. LILAS MOKE: Now Grace was a Thomas Jefferson sort of person; he's the one who said when you're angry count to 10. Zelda on the other hand preferred Mark Twain who said when you're angry count to four and when you're very angry, swear. So, I was going to read you from the book what Zelda said, but I left the book at home, so I'll adlib. She said when she was told that she has vision loss from macula degeneration and it wasn't correctable with glasses, she went home and smashed every dish in the house. She said, "I was screaming and crying and swearing and smashing dishes, and the kitchen floor was a mess." Now, I don't really encourage my patiets to go home and smash their dishes, but short-term anger can be healthy if it motivates you to actions, and Zelda's did. She went on to say that when she cleaned up her kitchen floor, she got on the phone and said OK, I need help. I need a vision rehab program, I need to know how I'm going to keep reading, I need to know how I'm going to keep shopping, and that inspired her to get moving and do something. She expressed her anger and work through it, which is healthy. Anger that he is buried and not express turns into depression, and depression and fear of the future are the enemies. You can learn to live well with vision loss but you cannot live well with depression and fear. And depression is common in vision lost.
  • [00:57:33.52] But it's important to know that the depression does not correlate with the level of vision loss; it correlates with the degree of function you have which means that people who have a system set up for accomplishing what they want to be able to do, in spite of vision lost, are not depressed. So preserving function is critical. And that is the mission of vision rehabilitation; to facilitate the transition from being a fully sighted person to living fully with partial sight in our sighted society. Vision rehabilitation at its core has been described as change management. Comprehensive rehabilition addresses every factor that compromises function with vision loss, and it uses a broad range of strategies adaptation and devices. Vision rehab starts with maximizing visoin, but even to know what that means, we have to talk about what vision is. Our common terminology phrases vision as kind of a dichotomy of sight and blindness, but vision is actually on a continuum from perfect vision to no vision, and the vast majority of people who don't have perfect vision have some level of vision, which we refer to as low vision or even better, as hard-of-seeing. The dictionary meaning of the term blindness and the understanding of sighted people at the term blindness means no sight. But the use of that word has been muddy ever since the 30's when the term legal blindness was adopted to identify those who couldn't be expected to make a living because of their vision, and at that time it was called economic blindness. Legal blindness includes everyone with visual acuity of 2200 or less, or an area of vision, as Dr. Moret was talking about, of 20 degrees or less.
  • [00:59:37.29] Now these demarcations were just arbitrary; there was no basis for then, in terms of function, and they prompted the famous comment in the 50's that more people are blinded by definition than any other cause. Now legal blindness creates a perception that the level of vision is accurately reflected by the 20/20 scale or the visual field. But those only describe part of the vision--the acuity and the field. And the acuty is just the size of a single black letter you see one a white eye chart. There are other important parameters of vision including contrast sensitivity, the pattern of resdiual vision, depth perception, and visual processing, and these are important for vision and for rehabilitation. With respect to contrast sensitivity, these photos have the same at level of detail in them; they just have gradually decreasing contrast sensitivity, and you see how much harder it is to see the one on the right than the one on the left. Lost of contrast sensitivity interferes with just common daily activity. Someone with poor contrast may be completely unable to pour coffee into a black cup, but into a white cup works fine. Contrast lost, even with good visual acuity, presents safety issues with things like steps and curves, which are the same as their surroundings. The curved brick area on the top right, for example, is actually a step, and that would be absolutely invisible to anyone with lost of contrast sensitivity. It also makes recognizing faces difficult which is confusing because faces are big, but their much bigger than a small button you might see on the floor. But they're hard to recognize because anyone's face is the same color as itself, so the features don't stand out. It also interferes with reading low contrast materials and newspapers are the best example of that. Now the flip side of contrast sensitivity lost is extra sensitivity to glare; both outside glare and inside clear as in this outside picture and the inside picture of a bathroom with glass doors and like reflecting off it. In fact, in a study of glaucoma patients, the majority of the mobility problems we're not because by missing area, they were caused by problems with lighting and glare. The area a vision that we have is affected differently by different diseases, and I'm going to illustrate this by superimposing different patterns on this picture of a the pedestrian street scene. Glaucoma when it's advanced affects peripheral field, as Dr. Moret said, before it affects the center, so advanced glaucoma would shrink the field out, all the way around, something like that. This makes it difficult to navigate the environment, so bumping into things would be a problem whereas until very late stages reading might not be a problem. With stroke on the left, which Dr. Moret referred to, eliminates one half of the area that you're seeing, demarcated vertically can be either the left half or the right half, but it's one half. So, that can have mobility problems as well and if it's in the right half it can have reading problems.
  • [01:03:03.75] Also, people with vision loss from strokes may in addition have some visual processing difficulty. Diabetes, on the right, has an unpredictable pattern and it's often described as swiss cheese because it's just random blurred areas. And of course diabetes out of control can also because total vision loss. Macular degeneration, on the other hand, affects the center of our vision exclusively, so it's saving grace is that you'll never lose all your vision. The center is the area we use when we're looking right at an object and therefore it doesn't affect mobility as much as glaucoma does, but it affects all detailed vision, and it doesn't take much loss to affect things like reading, writing, and driving. What's ironic in this is--and it's important for everybody with macular degeneration, everybody who knows somebody with it, or any other cause of central vision loss is--even though it has enormous impact and in fact can have more impact than losing both legs as illustrated by this gentleman with two prosthetic lower limbs, a motorcycle, it is absolutely invisible to the observer. You cannot look at someone and tell if they have macular degeneration. And then sometimes causes families and friends to underestimate or overestimate the amount of central vision loss or to misinterpret it as lack of cooperation or as a cognitive impairment. So, when grandma can see a small black button on the floor but you can't see her granddaughte's face, her daughter just decides that she can see what she wants to see. And when grandpa asks who that is standing in the driveway, his son says hm, must be losing his memory; he knows that neighbor perfectly well. And this misunderstanding is compounded if grandma or grandpa are among the 20 to 30% of people with vision loss, who experienced the phantom visions of Charles Bonnet Syndrome. And if they experience and tell anybody about it, which they often don't.
  • [01:05:08.28] Charles Bonnet was an 18th century Swiss naturalists who described his father-in-law, a retired magistrate, as being a sound mind but poor vision, and seeing repeated life-like images superimposed on the real world; and he perfectly well knew they were not there. So, we asked our patients to draw some of the things they saw or to describe to an artist what they saw. And on the left is it a wallpaper sort of pattern with the repeating baby's face in it. On the right, flowering trees, which our patients saw along the highway in Michigan in February. And these are two that our patient described to an artist; the ones on the left are Elizabethton figures who would appear in her living room from time to time, and she could describe them in every detail. The phantom images of Charles Bonnet Syndrome may move, but there is no sound, there's no smell, and there is no contact with the observer, with different shades then from other hallucinations. It can be like either seeing a painting if it's a wallpaper pattern or seeing a silent movie without the piano. On the right, our little girls which are patient described in white dresses with pink sashes and pink bows in their hair, playing in her yard. Now, this is the woman who couldn't see her own grandchildren playing in her yard, but these little girls were crystal clear. She said, "I know they're not real, but I kind of enjoy them." Now, true Charles Bonnet images are pleasant; they are common everyday objects, there pleasant, they're not threatening, and most people are not bothered by them, especially when I understand what they are. And this example in that, one of our patients saw a Canadian mountee in full dress in her living room and when we asked her if this ever frightened her just to see a man in our house--even though she knew it wasn't real--this 85 year old grandma said, "heck no; he's handsome."
  • [01:07:07.82] Now vision rehabilitation requires understanding the individuals' experience of vision loss and the parameters of residual vision that they have to work with, and then tailoring strategies to address their individual goals. And understanding the pattern of remaining vision is key. On the left, again, is advanced glaucoma and the right is macular degeneration. Those with peripheral field loss from glaucoma or strokes, or any other cause, have to master scanning skills. They have to be able to use a small area they have an see everything they need to see. And one of the ways that we do that is with the Dynavision which is a board mounted on a wall with small lights on it, that slash in random order, and the individual has to put them out by touching the light, and that puts the next one on. And it's a timed test so you can you track progress. It's also used, as you see on the right, to develop quick scanning skills for athletes. Now the challenge for central vision is different as it affects detail and therefore reading and other detailed tasks. So, two factors are important here. First, reading whole words and sentences is a whole different task from reading one letter at a time on an eye chart. And second, not all central vision loss is the same, and different patterns of central vision loss effect fluency differently. And to illustrate this, I'm going to show you some photos of maculas but to get oriented, if you look at the eyeball model on the top, that eye is facing you and you can see a little bit of the inside lining of the eyeball; all the sort of yellow color in that model. The macula is labelled there, but it is just a small area right in the back--dead center back--the the rest of the retina sees everything else that you're not looking right at, the macula sees what you're looking right at--the center of the macula--fovea, sees what you're looking right at. Now the pictures on the bottom shows just that macula. So, if you look at the picture on the left, the little dark spot on the right side of the picture is the optic nerve, which is right there, right next to the macula; the macula is right there. So, what the one on the left shows is a small blind spot; the terminology is DS and that's for dense scotoma and a scotoma is a blind spot. So, that is a small blind spot. That person, before he had anything wrong with his vision, would be using the center, right there, to see best with, but he can't use that spot, so he's moving up and looking above the target. So to see what he wants to see he needs to look above the object. Now the picture on the right shows a larger dense scotoma, a large blind spot. And here is another--this this one is a right eye, that one is a left eye, so the optic nerve's on the other side. So, this is the optic nerve, that's the big blind spot, the center of the macula would be right there. He can't use that spot, so he's moving over to where the red spot is. Now this situation would be difficult for reading because even if you magnify so that you can see with this spot, you're still bumping into that blind spot when you try to read. Reading Chinese may work fine because you're reading down, but reading English left to right would be problematic. So different strategies have to be developed for this person to read than for the other person to read.
  • [01:10:54.79] Now anyone who cannot use the center of the macula and is using a different area of their vision to see best has to learn how to use that efficiently, and to keep their focus on it, and to coordinate their hand with their eye. So I'm going to show you how this plays out in practice. Oh actually there's one more before I do that. This one is a doughnut-shaped blind spot on the left. The blind spot is all the way around the center. There's another little blind spot right in the center. This person had 20/50 visual acuity. That's enough to drive in Michigan and virtually any state; that's pretty good, but he's only got it in that little area. When the object is too big to fit in that little area then he moved back over here, so we went back and forth from this to that one, depending on the side. So, to show you how difficult this would be a read in spite of 20/50 vision, we superimposed that on a page of print, and you can see the only area he's got see with is right there; you can barely fit more than two or three letters. And if he says I'm having trouble reading and his daughter gives him a magnifier, that makes it worse because print's bigger, and then you can't even see part of a letter. So that's a different kind of problem and it has to be addressed differently with vision rehabilitation.
  • [01:12:20.92] Now I'm goin to show you how this plays out. Now this is a person--this is a photograph of the macula, the optic nerve is the thing over here. This area is macula. And from previous testing we know that this person's blind spot coincided with this big white spot that you can think of as a scar. And his next best spot, which is referred to as PRL for preferred retina locust, is over here, so his good side is to the left of this center. If he looks at an object straight on he won't see it at all. He's got it have the object in this spot, so the object has to be to the left of where he's looking. Now he was asked to cross out letters of the alphabet in order; first cross out the A you come to, then cross out a B, then cross out the C, and he consistently overshoots to the right, because he is looking to the right of the object he needs to see, and his hand is going where he's looking not to where the object he wants to find is. So, here, he wants to cross the A but he crosses out the B; he got to B pretty well. He was a little off on the C, he wants to cross out the D, and he's way over here, so he's always overshooting to the right. That affects your use of your hand for anything you might use it for, and that has to be learned and trained. Here's somebody with the PRL on the other side; he's got a big big area of scaring, the center is right here, his next best spot is over on this side of it. He asked to circle the words that are up above and he's trying circle the word head, and he gets the F on the left end of it, so he's overshooting left, because that's where he's looking in order to see the object. Because this is such an important factor influent reading--not such an important factor if you're just going to look at one letter at a time on an eye chart, but that's not what you want to do with your vision--it is important for fluent reading.
  • [01:14:33.98] So, we have a very rare and wonderful piece of equipment that allows us to make these diagrams and know where the blind spot is and where the next best spot is, and we've developed a system for training people to use it. And that's one of our occupational therapist doing that with the patient. We also, of course, work on the whole spectrum of devices for reading and writing, each of which has particularly advantages and disadvantages, and has to be match to the person who is going to use them and their individual needs and preferences. In our program we only dispense devices after they've been demonstrated to work successfully for the task for which they are desired, and that is usually after working with our occupational therapist with the devices so that no one byes something that is not useful. We have seven especially train occupational therapist, who are all certify low-vision therapist as well, and they do home visits throughout the metropolitan area to address the spectrum of home test. And just there to the side, the gentleman on the top right is my father, whose best vision was 2500 for macular degeneration, using screw driver.
  • [01:15:54.20] Lighting and glare control are very important issues and we, of course, address both of those for comfort and for safety, inside, outside, wherever it's a problem. We also address strategies for counting money, labelling appliances and medications, increasing contrast, organizing, and substituting hearing for vision with things like talking watches, glucometers, talking glucometers, talking books for example. It's important for those with vision loss to keep up their involvement in outside activities and in their community. And we address any of those that are of concern including what's shown here, for example, eating out with confidence, which is a real issue, shopping, bowling, and so forth. So far, I haven't had any of our OT's go play golf with patients, but they might like to do that as well. And in that regard, there is a blind golfers' league, you might be interested in knowing.
  • [01:16:49.91] We also evaluate and train patients in the use of bioptic telescopes for driving, which are allowed in Michigan, but to drive with them you have to pass two road tests. So, we do not dispense them until we have evaluated the patient enough so the patient and we are both quite convinced that they will pass the road test. For those who can't drive we help develop alternative transportation options and in fact, owning your own car is the most expensive way to travel. And of course we work on safe mobility with whatever is needed--no cane, just some safety tips: An umbrella as a depth finder, a walking stick, a support cane, a long weight cane; whatever works for the individual to keep them safe and moving about society. And one of our occupational therapists is also a specialist in orientation and mobility for the blind, so she can work with people who have, for example, severe glaucoma, vision loss, on safe mobility.
  • [01:17:52.52] So, does vision rehabilitation work? It is new in medicine. It has only been covered by medicare in Michigan since 1997 and nationally since 2002. So, there hasn't been a lot of time for many outcome studies; never the less, the a few that are there have shown positive results. There are studies now going on in Alabama and Johns Hopkins. The VA has already completed a study, and we are now doing a study also along with Harvard and enrolling patients, and ours is the first one that actually has placebo control. Until we get our study results we have a collection of voluntary testimonials from patients about our program and our OT's. And my favorite one is the last one, Annie, one of our OT's, "Is better than Prozac".
  • [01:18:48.50] So, to you who have been diagnosed with an eye disease, don't lose heart; there is help out there, there is life after vision loss. And for those of you who already have lost the vision I urge you to embraced the opportunity to learn new ways to do things. And reach out and get the help you need to keep the independence. Now in that regard we know that being active in sighted world, when you are partially sighted, requires a little risk-taking, physical risks, yes, but actually social risks are even more of concern for many people. A few examples--Francine, who had macula degeneration and was a great cook, but one eveing she served her guest dinner, and dessert was cherry pie, and it turned out to be made out of kidney beans because she mixed up the cans. And she said, just as you did, she said we all had a good laugh about it, and none of her friends loved her any less for that. My father would occasionally say, "Well, I asked the mannequin for directions today."
  • [01:19:57.27] [LAUGHTER] DR.
  • [01:19:57.47] LILAS MOKE: And he'd just chuckle about that. And I was going to read you the comments of one of our patients, retired attorney, who had very advanced AMD, but I forgot the book, so I will adlib it. He said I'm and over achiever and that has gotten me far in life, but sometimes I forget about a sense of humor, so with this macula degeneration I decided to try to work on that, so he said. My wife Rachel and I went to a party and she wore black and white patent leather shoes, so I went looking for her in the party. And those of you who have macular degeneration know that he couldn't recognize her in a crowd, but he could see black and white shoes off to the side. So he said I found a pair of black and white patent leater shoes and I said to this woman "Are you my wife?" She said "I certainly hope not."
  • [01:20:52.23] [LAUGHTER]
  • [01:20:53.72] DR. LILAS MOKE: And he said, "You don't know what you're missing."
  • [01:20:57.15] [LAUGHTER]
  • [01:20:58.68] DR. LILAS MOKE: And then he went on to say later in the party, Rachel found me eating cat food out of a little bowl on the kitchen and she said what are you doing. And he said it looks just like nuts and crackers. And he said we had a good laugh about that. So, as Francine and my father and our lawyer friend knew, you are much more than your eyes. Your friends don't love you because of the quality of your vision, and your value to yourself, your family, your friends, and your community does not fade with fading eyesight. And it does not define what you can do with the proper strategies and tools and resources, and training. If you can keep a sense of humor and laugh at your foibles, which we all have, it will make living lighter, and it will put vision loss in perspective as part of your life but not the definition of your life.
  • [01:21:57.32] And finally, as a little prince said, keep in mind that what is essential is invisible to the human eye.
  • [01:22:03.69] [APPLAUSE]
  • [01:22:09.11] DOREEN SHAW: Although we're supposed to have concluded four minutes ago, I was just so absorbed in the topic that--and hopefully our guest can stay for maybe ten minutes, and will take some questions from the audience. Why don't you go ahead. Anyone has questions? You're go.
  • [01:22:31.73] SPEAKER 1: I was just diagnosis glaucoma and my eye doctor did not tell me anything except that it was the pressure on the eye, and he gave me some samples of medicine and said come back in six months. I'm concerned that in six months it might not be as good is it is now. And secondly, I went to my regular doctor and she said, "You should be taking that"; she said, "Here, let me prescribe another medicin", which she did. What am I going to do?
  • [01:23:16.20] DR. SEIKO MORET: One thing that I always--being at a university--I often get referred patients to me. I do have some patients who I make a diagnosis; that's not typical for me. I think it's very important that you feel that you have a relationship with your physician, that you feel you can communicate with him and her. For my usual practice, different physicians have different practices, when I initiate treatment, I like to make sure to follow up with the patient. My typical follow-up is usually between three to five weeks; that that's my typical follow-up. And I think since you have expressed concerns, I think it would be very very important for you just to call the office and say can I have a sooner appointment. I also let my patients know that I don't know everything. If they feel they want to have a second opinion, I also let them have a second opinion and can make recommendations. So, I think it's very important that you feel like you can communicate with your provider, whether it's an eye doctor somebody else. You're welcome.
  • [01:24:27.15] SPEAKER 2: Hi. There are several studies that have shown that patients with glaucoma have a terrible time getting drops in their eyes and even though they think their getting them in their eyes almost a third of the thime their not getting adequate amounts in them. Is there any work being done to try to develope different delivery systems to make sure that the drops get into the eyes?
  • [01:24:52.55] DR. SEIKO MORET: Yes, that's very hard and probably Dr. Moke can attest to that too. The basic question I'm--Im sorry, maybe I should repeat the questions is--it's hard to take medication, and it's especially very hard to take eye drops. For a new patient to me, I give the introduction of how to try to take medications--wash your hands first, pull down the lower eyelid, maybe even use a mirror. Then I always call my technicians in and I asked them to come and please spend more time; the education component is critical. But still, it's very difficult for some patients to be able to get their medications and then I have to express my frustration with some insurance companies where they say you cannot get more medication. So, it's like my patient has spilled half their drops on there eye; they cannot get them in there eye. But there are some--well the issue is they said no, you can't refill the medication; it's too soon. That bottle should hold 30 days' supply, you're coming back at 20 days; you can't have it. The answer is I guess no. There are some devices where you can insert certain--almost like you have a funnel, but it has a very wide rim so you don't poke your eye, that you've placed it back then aim and squeeze. But even that's difficult to manipulate, I don't know if you--
  • [01:26:27.66] DR. LILAS MOKE: There are some devices that help some people that comes in a little form and if you lie down, their a better chance of getting it in, but it's an ongoing problem.
  • [01:26:39.40] DR. SEIKO MORET: There is some research being done though in what we call alternative delivery. Some drug companies are in trials right now, having these dissolvable plugs to place in the tear duct to deliver the medication to the eye, and then maybe you only have to have that inserted once a month; something like that. There are also development surgical devices, but I'm not too keen about having a surgery device developed to deliver the medications. So, we need better ways to managed glaucoma.
  • [01:27:14.49] DR. LILAS MOKE: One of the strategies that some of our patients use is to lie down and aim the drop at the center, right next year nose, and then turn your head, and it will fall into your eye, so there is a little less drips down your cheek that way.
  • [01:27:31.93] SPEAKER 1: [INAUDIBLE] Is that all you can do for it is just take those eyedrops? DR. SEIKO MORET: Well it it's interesting. The question was for glaucoma--are drops the only way to treat it? In America, we tend to use medications first, but my chairmen, Dr. paul Lichter, being very well experienced and also being aware also of what other countries do, we tend to be pretty conservative in US. Our counterparts in Europe tend to intervene with surgery much sooner. And so he ran a study to look at if you are diagnosed with glaucoma, which is better? Surgery first or medication? It turns out that with our newer medications now, the medications are very effective in lowering pressure. Surgery is a little better, but also surgery has risks up problems;, what we call complication. So, we have to weigh the risks and benefits when we advise our patients which way to go. I would say still the majority of us consider eye medications first, but I talked very carefully with some of my patience. Our riight, some of them will say, "Doc, I don't want to take any medication; forget it!" So, I said OK. So, then I talk about laser approaches, to see if that's an approach. And then I have a serious communication regarding surgery, and I don't mean to scare them, but I tell them the risk of the surgery, what the expected, I guess, longevity of those surgeries or success are; and they're not lifelong. As I said that child who was seven years old. There's going to be three generations of ophthamologists--two after me I hope, but there's going to be several generations of ophthalmologists after me that are going to be responsible for him. So, I always have to think of the next step for that patience.
  • [01:29:34.34] [INAUDIBLE]
  • [01:29:39.24] DR. SEIKO MORET: Oh, oral medication? Yes, there are some pills to take; they have a lot of side effects, and so that why we tend to not use them as much anymore.
  • [01:29:49.92] CELESTE: Questions? Well, I'd like to think very much being here this evening and thank you all in the audience for coming too.
  • [01:30:04.00] [MUSIC]
  • [01:30:12.87]
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April 15, 2010 at the Downtown Library: Multi-Purpose Room

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