Experts help us understand vision loss from age-related macular degeneration by explaining the complex eye-brain connection. Read on to learn more.
“In a way, your eye is a direct extension of your brain,” a part of the central nervous system, says Timothy G. Murray, MD, a past president of the American Society of Retina Specialists.
In order to understand “wet” age-related macular degeneration (wAMD), you need to understand the relationship between your eye, optic nerve, and brain, and how they all work together.
Seeing isn’t an event but a process. Light enters the cornea, pupil, and lens at the front of your eye, and moves to the retina, a thin layer of tissue at the back of your eye. From there, photoreceptor cells turn the light into electrical signals that travel up the optic nerve to the visual cortex in your brain, which interprets the information. Two-thirds of your brain is devoted to this visual process and pathway.
“Starting around the age of 60 or so, little deposits will build up underneath the retinal cells,” says Robert W. Wong, MD, of Austin Retina Specialists, and affiliate faculty in the Department of Ophthalmology at the University of Texas at Austin Dell Medical School. “These retinal deposits are called drusen. These are basically the waste products of the retinal photoreceptor cells.” Drusen are made of proteins, lipids, and other cellular debris.
Normally, your body removes these waste products twice a day, explains Wong, but as your metabolism slows with age, the drusen deposits can accumulate. This buildup usually occurs in the macula, the very center of the retina, and can cause mild distortions in your vision. This is called “dry” AMD. Like glaucoma, dry AMD can take years to progress. Wet AMD, however, is a different story.
Wet AMD is a less common but faster progressing condition than dry AMD (only 10% to 15% of AMD cases are wet), and can cause vision loss in just a few months. Wet AMD begins as dry AMD, but then an abnormality occurs. Blood vessels begin to grow where they don’t belong, in the macula. These vessels leak blood and other fluids, which causes scarring, particularly in the fovea, the very center of the macula, where vision is usually clearest.
Although there’s no cure for dry or wet AMD, treatments are available. For dry AMD, a vitamin formulation called AREDS-II can help slow progression. For wet AMD, a treatment called anti-vascular endothelial growth factor (anti-VEGF) therapy is available to slow progression and prevent further vision loss.
A monitoring tool called optical coherence tomography (OCT) has also made possible the early detection of the conversion from dry to wet AMD, enabling earlier intervention. Murray calls both anti-VEGF therapy and OCT technology “game changers” in the fight against blindness from this condition.
The brain does not appear to cause wet AMD, says neuro-ophthalmologist Joshua Pasol, MD, an associate professor of clinical ophthalmology at Bascom Palmer Eye Institute of the University of Miami Miller School of Medicine, but it does respond to it.
Since wet AMD causes vision loss in the center of your eye, your brain–specifically the occipital lobe that receives visual data–attempts to compensate by instructing you to use your peripheral (side) vision more.
Visual hallucinations are another way your brain attempts to compensate for gaps in your vision, says Dr. Wong. Experiencing hallucinations upon waking is called Charles Bonnet Syndrome. Your brain is essentially trying to fill in missing retinal messages by making you “see” images that aren’t there. This effect can occur not only from advanced wet AMD but also from other conditions that lead to blindness.
Speak with your eye health provider about changes in your eyesight. The sooner issues are identified, the sooner you can intervene and preserve your vision.
*Boyle, E. L. (2021, July 12). This Is Your Brain on Wet AMD. HealthCentral. https://www.healthcentral.com/article/wet-amd-and-the-brain
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