Lee Allen was an art student at the University of Iowa when Grant Wood offered him a job. By the time Lee had completed his studies with Grant Wood in the 1930's, he was an accomplished artist and draftsman. He later applied these skills to medical illustration. He became an outstanding ophthalmic medical illustrator and photographer. In midlife, he blended his keen skills of observation, attention to detail, and artistry with plastic polymer technology and became a master maker of artificial eyes, an ocularist. At a time when most men begin to think of retirement, perhaps to paint Iowa landscapes, Lee Allen left the security of the university to establish a laboratory and training program to enhance the art and craft of making artificial eyes. Only after Lee and his students gained international recognition for the technique of making the plastic eyes, that he had popularized, did he turn his attention once more to painting his beloved Iowa, and then to recording the changes in his own vision which he observed over the following decade.

The Hole In My Vision provides an unusual view through the author's eyes of age-related macular degeneration, a very common cause of blindness. In this work Lee Allen offers us a glimpse of what the patient can see looking out at the world through a damaged eye, and we get to compare this to the view the doctor observes through an ophthalmoscope while looking into the same eye.

What makes this effort truly unique is that Lee brought to the task a lifetime of related skills -- skills in drawing, color analysis, teaching, and anatomical knowledge -- all supported by a driving need to understand what he was seeing. He has brought this conjunction of talent, experience, disease process, and will power to focus on the visual disturbances experienced by millions of people throughout the world who also suffer from macular degeneration. He has taken the trouble to study and draw the entoptic phenomena (the internal images) that are experienced by people with macular degeneration. Lee Allen draws and then describes his own visual experience with the help of his long-time colleague Dr. Stan Thompson, emeritus professor of ophthalmology, and his personal ophthalmologist Dr. Jim Folk. This is an illustrated diary of an artist and scientist whose failing vision many of us can relate to personally, through our families or through our patients.

Age-related macular degeneration (AMD) is the most common cause of blindness in industrial nations. It is rarely detected before 55-years of age and seldom causes visual impairment before that age, but 10 to 15 percent of individuals over the age of 65 have signs of AMD and by age 70 the number increases to 33 percent. As our society ages, the prevalence of age-related macular degeneration will increase, and in many families, it will have an increasing impact on the quality of life.

The hallmark of AMD is macular drusen, deposits underneath the retina that are visible through the ophthalmoscope. Most people with AMD experience a very gradual loss of vision over many years. This is the result of regional atrophy of the retinal pigment epithelium, a layer of cells that covers the outer surface of the retina. These critical cells slowly begin to die, especially the ones near the drusen. At first the changes are so subtle that they often go unnoticed for years. Even if this so-called dry form of AMD (that accounts for 90 percent of people with AMD) is recognized, there is, at the moment, no way of stopping the process.

Vitamins, zinc, supplemental metals, antioxidants, Bilberry juice, herbs, radiation, hyperbaric oxygen, transcutaneous electrical stimulation, and plasmapheresis have been tried in the hope of halting this process, but none have ever been demonstrated scientifically to have any value in preventing progression of age-related macular degeneration.

The less common form of AMD, the wet form, is associated with a tangled nest of tiny abnormal blood vessels that sprout (subretinal neovascularization) from the vascular blood vessel layer called the choroid behind the retina. From these new vessels under the retina (this subretinal neovascularization), fragile blood vessels grow into the retina, then they may leak fluid or bleed. The resultant hemorrhage and lipid deposits first distort and then obliterate the central part of the retina, producing a hole in the patient's vision.

Laser photocoagulation of some of these nests of blood vessels (neovascular membranes) may prevent further loss of vision, but they often grow again. This is also true of photodynamic therapy (the photocoagulation of new blood vessels after they have been made vulnerable by an injected drug).

AMD of the wet variety (that is, the kind with new blood vessels) can be treated surgically either by moving the center of the macula (so-called macular translocation) or by removal of abnormal blood vessels from beneath the macula. Both procedures have had limited success and are fraught with many potential complications; they are costly, and are an impractical solution for combating blindness in millions of people. Retinal tissue transplantation is another procedure in the earliest stages of development and it is impractical for the same reasons.

Dry (atrophic) AMD and wet (neovascular) AMD are usually separate and distinct conditions; however, individuals may have one form in one eye, and the other kind in the other eye. In some individuals, the atrophic form can evolve into the neovascular form.

While no cure is available at the present, the future is promising. Through molecular and cell biology it should be possible to identify those at risk of developing AMD decades before the onset of symptoms and to provide gene-directed therapy that may delay the onset of visual symptoms and blindness indefinitely. This is the aim of vision scientists, ophthalmologists, and the hope of the public nearly 150 years following the discovery of drusen with the ophthalmoscope.

Thomas A. Weingeist, Ph.D., M.D.