Posts Tagged ‘age-related macular degeneration’

Macular disease, cataracts and art

Thursday, October 24th, 2013

My wife and I are supporters of two art museums, one locally and the other in Denver. I also have a personal interest in eye problems, especially cataracts and macular disease, as my father had lost an eye as an intern (a paper cut led to an infection and, in those days, before antibiotics, there was concern about the other eye developing problems, a medical issue called sympathetic ophthalmia). In his late 80s he had a cataract in his remaining eye and, when he was examined by an ophthalmologist at the Cleveland Clinic, was found to have macular degeneration, a chronic eye disease  usually seen in people over 50.

Someday my visions may deteriorate to this point.

Someday my visions may deteriorate to this point.

I became aware, as I read about Dad's problem, that one day it might become mine as well; one of the risk factors for macular degeneration is a family history of the disease.

I've pasted in a list of symptoms from this condition (copied from a Mayo Clinic website).

  • The need for brighter light when reading or doing close work
  • Increasing difficulty adapting to low light levels, such as when entering a dimly lit restaurant
  • Increasing blurriness of printed words
  • A decrease in the intensity or brightness of colors
  • Difficulty recognizing faces
  • A gradual increase in the haziness of your central or overall vision
  • Crooked central vision
  • A blurred or blind spot in the center of your field of vision
  • Hallucinations of geometric shapes or people, in case of advanced macular degeneration

The National Eye Institute, a branch of the NIH, has a fact sheet on age-related macular degeneration (AMD) that's worth looking at if you or someone in your family develops this problem. I'll mention a few things from that website as AMD is a major cause of vision loss in older adults. To begin with the macula is the part of your eyes that gives you the sharpest, most detailed vision. It's the extremely sensitive part of the retina, the layer of tissue  at the back of your eye that responds to light, converting images, focused by the eye's lens on this equivalent of camera film, into electrical signals that travel via the optic nerve to the brain. If the macula is damaged, fine points of these images become less clear.

If this happens to a non-artist, someone who doesn't make their living through images they put into a form that others can enjoy, it still leads to less sharp vision. You may have problems reading, driving or recognizing an image such as a face. Since your peripheral vision isn't affected, you'll probably be able to walk around without major difficulty.

But image that you're an artist. You gradually realize your vision is becoming less clear. You used to be able to read an eye chart at the 20/20 level, meaning you can read the same row of small letters on the chart at 20 feet which those with normal vision can. Now your visual acuity, measured when you see your eye specialist, is slipping and you worry that it will affect your ability to paint as well as you once did.

Having 20/20 eyesight does not necessarily mean perfect vision. 20/20 vision only indicates the sharpness or clarity of vision at a distance. There are other important vision skills, including peripheral awareness or side vision, eye coordination, depth perception, focusing ability and color vision that contribute to your overall visual ability.

Some people can see well at a distance, but are unable to bring nearer objects into focus. This condition can be caused by hyperopia (farsightedness) or presbyopia (loss of focusing ability). Others can see items that are close, but cannot see those far away. This condition may be caused by myopia (nearsightedness).

I've written about these medical problems before, but was riveted by a pair of articles I found in two AMA publications yesterday. A Stanford eye surgeon, Dr. Michael F. Marmor, just published a supurb article on Edgar Degas' progressive loss of vision in his later years. Degas was born in Paris in 1834 and died there in 1917. His painting altered from 1860 , when he had essentially normal vision, to 1870 and beyond  when first one eye, then the other progressively lost visual acuity. By 1897 he was seeing at a 20/200 level; that means he could would have to be twenty feet away from an eye chart to read the letters that someone with normal vision could read from 200 feet away.

The style and details of his paintings, especially his pastels, have been shown to change as Degas' eye problems progressed, but Dr. Marmor's article calls our attention to one oil painting, Scene from the Steeplechase: The Fallen Jockey. Here's a link to the painting in the National Gallery of Art; it was originally painted in 1866 and reworked by the artist in 1880-81 and again in 1896 with considerable changes made which Dr. Marmor shows can be linked to Degas' declining visual acuity.

A number of other significant artists have demonstrated visual loss in their work. An April, 2007 article in ScienceDaily focuses on Dr. Marmor's work, mentioning he's authored two books on art and eye sight: Degas Through His Own Eyes and The Artists's Eye (I've ordered a copy of the latter book through Amazon).

The Blind with Camera School of Photography website mentions a number of other famous figures from the art world who struggled with visual issues. Among those were El Greco, Rembrandt, Van Gogh, Paul Cezanne, Claude Monet, Mary Cassatt, Camille Pissarro and Auguste Renoir. Georgia O'Keeffe, who lived to the age of 98, also suffered with significant eye disease in her later years; her almost complete loss of eyesight and ill health during the last fifteen years of her life significantly curtailed her artistic productivity. Her eye problems began in 1968, and by 1971 macular degeneration caused her to lose all her central vision.

How is this honeybee similar to Monet?

How is this honeybee similar to Monet?

Monet had cataracts which not only diminished his visual acuity, but also affected his perception of colors. He resisted having surgery, but eventually decided to have one cataract removed. After the operation, according to science writer Carl Zimmer's review of the San Francisco Exploratorium's free  publication, Color Uncovered, Monet, like honeybees, was able to see ultraviolet light (normally filtered out by the lens of your eye) and painted water lilies a pale blue. Bees are guided to pollen by light signals we are unable to perceive; Monet had lost a lens to surgery, but gained a spectrum of light perception the rest of us lack.

I have zero talent as a visual artist, but after bilateral cataract surgery my vision is correctable to 20/20...for now.




The Eyes have it: Part two: diseases of the cornea and retina

Wednesday, June 19th, 2013

My own eye history is complex: I found out I was nearsighted at age eight while attending a baseball game with my folks. They mentioned the score and I asked how they knew what it was.

"Just read the scoreboard," Dad said.

My eyesight isn't perfect, but I haven't gotten to this stage yet

My eyesight isn't perfect, but I haven't gotten to this stage yet

"What scoreboard?"

Much later, after years of wearing glasses (now they're bifocals), I was diagnosed as having a corneal disease...and that was even more years before the cataracts.

In my last post I outlined the anatomy and physiology of vision so that I could focus (pun intended) on diseases of the cornea and also on age-related macular degeneration this time.

In my prior post on the eye, I translated dystrophy as "it grew incorrectly," but "dys" comes from the Latin for "bad" and "trohe" from the Greek for "food," so poorly or inadequately nourished perhaps would be a better rendering for the term. A National Eye Institute document I provided a link to previously, "Facts about the Cornea and Corneal Diseases,"  says all of these dystrophies share a number of traits. They are usually inherited, affect both eyes equally, aren't caused by diet or injury, progress gradually and aren't related to systemic diseases, those that affect the rest of the body. They define a corneal dystrophy as "a condition in which one or more parts of the cornea lose their normal clarity due to a buildup of cloudy material."

Let's start with keratoconus, an abnormality of the cornea that usually affects both eyes, most frequently occurs in those who are ages 10 to 25 and slowly progresses over roughly a decade. It results in thinning and bulging of the cornea which forms a cone shape. This is a relatively uncommon disease affecting one in 2,000 of us and in its early stages can often be corrected with glasses or soft contact lenses.

Later on other kinds of contacts or even corneal transplantation may be required. If the patent gets such a transplant, its success rate is quite high with one estimate of an 89% positive outcome lasting ten or more years. An experimental treatment called collagen cross-linking is being evaluated around the world with clinical trials in multiple centers in the United States.

Less than 10% of those who have keratoconus also have a family history of the disease. Others may have had an eye injury, have other eye diseases, or unlike most other corneal problems, their keratoconus may be associated with systemic disorders including Down Syndrome.

My mother was said to have Fuchs' dystrophy, a slowly progressive corneal problem that normally affects both eyes, rarely alters vision until those who have it are in their 50s and 60s, and causes early-morning blurring that gradually clears as the day progresses. One layer of cells in the cornea, for unknown reasons, slowly dies off. They normally help pump water out of structure and, in their absence, the cornea swells, distorting vision.

Fuchs' is a major problem and some affected by this disease require advanced treatments including corneal transplantation. The success rate for this is reasonably good (73% after ten years), but waiting for donor tissue to become available is an issue.

I have map-dot-fingerprint (MDFD) dystrophy, according to most sources the most common of over 20 conditions in which parts of the cornea lose their usual clearness as cloudy materials pile up.

MDFD usually hits adults between the ages of 40 and 70, but can develop earlier. I remember cutting my right eye with a paper towel in 1971 when I was 30. It healed slowly and I had recurring episodes of eye pain, especially when I first woke up, over a period of four or five months. I'd bet that was my first hint of MDFD which typically will have flares over a few years and then go away without any long-last effect on vision.

A 2012 Medscape article says MDFD is rarely hereditary and may better be described as a corneal degeneration. Estimates of its prevalence in the general population range widely, from 2 to 43%. Like me, up to a third of those with MDFD have repeated early morning corneal tears/rips termed corneal erosions. They happen because in MDFD the outermost of the cornea's five layers of tissue, the epithelium, doesn't stay correctly attached to the layer below.

Since your eyes naturally get dry at night, your eyelid may stick to the epithelium and when you first awake and open your eyes, the not-well-attached epithelium can tear off casing mild to even severe pain.

I'm going to move to the back of the eye and age-related macular degeneration (AMD). Remember that light from images we see passes through the lens and goes to the retina, a light-sensitive layer of cells that line the inner surface of the eye. As the light impinges on these cells, two types of them react to the stimulus with a series of chemical/electrical events that eventually trigger nerve impulses sent through the optic nerve to the visual centers of the brain.  One kind is called rods and they are most important in dim light and provide our black and white vision. The other kind are termed cones and those are useful in our color perception and in daytime vision. I'll ignore a third type of receptor cells, important in reflexive responses to bright daylight.

The macula is the dull round area slightly off-center

The macula is the dull round area slightly off-center

Near the center of a retina is a small, oval-shaped spot called the macula (Latin for "spot") that is critical for high-resolution vision. It's yellow in color, absorbs UV and blue light and is sometimes referred to as a natural sunblock protecting this highly-important area of the retina. The yellow color comes from two chemicals, lutein and zeaxanthin, which are derived from our diet. They are members of the carotenoids, a group of greater than 700 fat-soluble nutrients that provide the color in foods like carrots, pumpkins, sweet potatoes and other yellow, red, orange and deep green fruits and vegetables. Some of these, but by no means all, are converted to vitamin A or retinol, its active form, in the body.

AMD is the leading cause of major loss of vision in those of us over 50, accounting for more than half of all blindness in the United States. A major project, The Age-related Eye Disease Study (AREDS) has shown that taking some supplements can reduce the risk of progression to advanced AMD by 25% at 5 years. I've been taking a half dose of one of these for some years. Now a recent article in JAMA, "Lutein +Zeaxanthin and Omega-3 Fatty Acids for Age-Related Macular Degenerationpart of the followup study, AREDS2, looked at specific components of those formulations of antioxidant vitamins and minerals.

Their conclusion was adding the two carotenoids, lutein and zeaxanthin (L&Z), and the omega-3s  to the basic ingredients didn't seem to offer a further reduction in risk of AMD, but  L&Z might lower the risk of lung cancer in former smokers.

I'm not changing the pill I now take. I don't think ingesting the equivalent of a little extra carrot or sweet potato will hurt me.


The Eyes have it: part one: Anatomy and Physiology

Friday, June 14th, 2013

I already have an eye disease, a corneal problem called map-dot-fingerprint dystrophy (translated as "it grew incorrectly"), but I'm much more concerned about the one my father had late in life, age-related macular degeneration. I need to walk you through the anatomy of the eye (How's that for a mixed metaphor?) before I can outline what either of those ophthalmologic problems are and what can be done to correct, treat or prevent them.

The National Eye Institute has a discussion of the visual system, at a level most appropriate for kids, but very worth viewing and listening to by anyone who is visually oriented in their learning style. I think it's the one link I'd suggest clicking on if you want an elementary, but accurate audio-pictorial description of how our vision works.

I'll also give you a link to the WebMD's Eye Health Center, which has a very nice picture of the parts of the eye and links to many eye diseases, but eventually I plan only write in any detail about two of those parts, the cornea and the retina.

a cross section of the human eyeWe each have two eyes, unlike spiders which usually have eight (I wonder how many Spiderman has). Each eye sees a slightly different view of an object, so we have stereoscopic vision, important in judging distance and in fine manipulation. The front of our eyes have a pigmented part called the iris, a clear domelike structure called the cornea over the iris and an opening in the iris (the pupil) to let light through.The size of the pupil varies, as we've all noticed, with how bright the light is. You can't see the conjunctiva, which is a covering for all of the rest of the front part of the eye except for the cornea. Then a tough fibrous white membrane called the sclera surrounds most of the eyeball  posterior to the cornea.

When you're looking at something, for instance, your family dog, light representing that object enters your eyes through your pupils, passes through a lens (this is a focusing device) and through a gel-like material called the vitreous humor to the retina, the light-sensitive tissue in the back of the eyeball.

The picture of the object you're looking at is inverted by the time it gets to the retina whose cells convert the light into electrics impulses which are then carried via the optic nerve to a part of the brain called the visual cortex. That's located way in the back of your skull in the occipital lobe of the brain (if you feel the back of your head, you'll note a bump called the occiput).

Then things get very complicated, much more so than I want to delve into, but if you're really interested here's a link to a 24-page convoluted article I found. The author, a professor at Weber State University, made the statement about six years ago that if we want to fully understand what happens when the signal leaves the retina, there are two fundamental questions: "What are the discrete anatomical pathways that carry the signal?" and "What information do the signals actually carry?"

His conclusion was that the answers to these questions do not (currently) exist.

So let's go back to the two parts of the eye that I personally have been most concerned about and start with the National Eye Institute' comprehensive online discussion, Facts About The Cornea and Corneal Disease. I'd term this article "Everything you might possibly want to know about the cornea and lots more," so I'll attempt to abstract some salient points.

First the cornea, in order for us to have good vision, must be free of any cloudy or opaque areas, so unlike most parts of our bodies, it doesn't have any blood vessels. How does it get its nourishment? Both our tears and the vitreous humour (British spelling), the gel-like watery substance that fills the eyeball between the lens and the retina, play a role in keeping our corneas healthy.

The cornea is both clear and strong and has several functions: it protects the eye from dust and germs and, at the same time acts as an outer lens to help focus light. It also screens out some of the potentially damaging ultraviolet (UV) light in sunlight.

The cornea is frequently misshapen and if it is curved too much or the eye is overly long, objects at a distance don't focus on the retina. So about 25% of us, those who have this corneal issue, are nearsighted (myopic). The opposite causes farsightedness (hyperopia) and that's seen in 5 to 10% of both kids and adults.

glasses can often correct myopia, hyperopia or astigmatism

glasses can often correct myopia, hyperopia or astigmatism

Two-thirds of Americans who are myopic (and some who are hyperopic) also have a condition called astigmatism where the curvature of the cornea isn't smooth, so both near and distant objects appear blurry. This often is correctable by glasses, but special contact lenses or laser surgery are sometimes needed.

Those of us who are allergic to pollen can note corneal irritation, especially during dry, hot weather and may have tearing, corneal redness, itching or other symptoms. Most of the time those problems don't necessitate medical visits. Antihistamine decongestant eyedrops often reduce our symptoms. Some of us are allergic to animal hair (dander), cosmetics, or medications and those substances or even rubbing/touching your eyes after using soaps, chemicals or applying nail polish can cause a corneal reaction.

Minor injuries to the cornea may be self-healing, but more severe ones clearly require an eye professional's attention. Similarly corneal infections from a poke in the eye or a contaminated contact lens may necessitate professional help.

As I mentioned before, tears are important for a healthy cornea so dry eye, a condition more common in women, particularly after menopause, may require the use of artificial tears and may be helped by using humidifiers and wrap-around glasses for outdoor wear. Interestingly, people who have dry eye may sometimes have tears running down their faces.

I'll get to corneal dystrophies and macular problems in my next post.






Should I be taking aspirin?

Wednesday, January 30th, 2013

I take a dose equivalent to 1/4 tablet of aspirin

One of our friends recently told my wife she'd stopped taking aspirin after a news report linked regular use of the medication to macular degeneration. We've both taken 81 mg of aspirin a day and, after I'd heard that people may not absorb the enteric coated form well (and I couldn't find any other form in that size at the local drugstore), I'd ordered ten bottles of chewable orange-flavored aspirin online from Amazon.

Then I decided to read the medical reports that our friend's recommendation had been based on. She doesn't have a medical background and hadn't looked at the original data, but instead had seen a warning in a newspaper article. Let's start at The New York Times blog. On Dec 12, 2012 they published an article by Anahad O'Conner titled "Aspirin Tied To Rare Eye Disorder."

It's a very well-worded article written by a 31-year-old, Yale-educated Times reporter who writes a weekly science column and has published two books He notes the article he based his piece on was from JAMA with the lead author, Dr. Barbara Klein, being a professor of ophthalmology at the University of Wisconsin, Madison. Since I'm a UW graduate (BS 1963, MD 1966), I was particularly interested in her study.

It used data from the Beaver Dam Eye Study, started in 1988-1990 and concluded in 2010. O'Connor very appropriately noted this was an observational study, not a prospective, controlled research project. In other words a group of ~5,000, aged 43 to 84, agreed to have regular eye exams and reports were published after the 5-, 10-, 15- and 20-year followups.More than 300 publications have resulted from this project with data supporting a relationship of cataracts and age-related macular degeneration (AMD) to cigarette smoking.

Klein's paper stated that an estimated 19.3% of US adults take aspirin on a regular basis. It's commonly recommended for anyone who has had a heart attack (secondary prevention), but many   of us who've never had evidence of coronary vascular disease also take aspirin. This is primary prevention and is controversial with some data suggesting reduction of heart attacks in men over 45, but not women, although they may have a 17% reduction in stroke incidence.

A senior who has AMD may need a magnifying glass.

A January 21,2013 article from an Australian group reported a two-fold increase in AMD of a particular type, independent of smoking habits. Nearly a quarter of regular long-term aspirin users developed neovascular AMD, two and a half times the percentage of those who did not regularly take aspirin.

A 2001 paper in the Archives of Ophthalmology reported a randomized, double-masked, placebo-controlled study of low dose aspirin (one adult tablet every other day) plus 50 milligrams of beta carotene (a vitamin A precursor rated possibly effective in treating advanced AMD) among over 20,000 US male physicians aged 30 to 84 in 1982. The study was stopped after ~5 years due to a statistically extreme reduction (44%) in first heart attacks. There were fewer cases of AMD in those taking low-dose aspirin than in those who got the placebo.

There's also some data supporting aspirin's role in cancer prevention, especially in malignancies of the colon. Here the benefit was unrelated to aspirin dose (75 mg/day and up), but increased with age.

So let me look at my own risks: my dad had a large polyp in the earliest part of the colon, an area hard to see even on colonoscopy. It was initially felt to be benign, but later had some areas of low-grade malignancy. He also had macular degeneration in his remaining eye  diagnosed at age 90+ (the other eye having been removed nearly sixty years previously after a bad cut and a subsequent infection). My brother died of a heart attack at age 57 and my mother had a heart attack at age 74 with a cardiac arrest; (Dad resuscitated her and she lived to age 90).

The editorial that accompanied the recent JAMA article is thoughtful and impressive. Its title was "Relationship of Aspirin Use With Age-Related Macular Degeneration: Association or Causation?" and it concludes "From a purely science-of-medicine perspective, the strength of evidence is not sufficiently robust to be clinically directive." It then switches to a different viewpoint, the art-of-medicine perspective, saying maintaining the status quo is currently the most prudent approach, especially in secondary prevention (someone who has already had a cardiovascular event). For those of us who haven't, the risks versus benefits should be individualized based on our own medical history and value judgement.

I'm going to discuss this with my own physician but not stop taking a chewable 81 mg aspirin daily until I do.