We all know that we have a blind spot because there are no photoreceptors located at the optic nerve. The facinating thing is when you look at an object you don’t see part of it missing, correct? If you do, please go see an optometrist ASAP!
Why do we not see a hole in our vision? The brain is amazing when it comes to visual perception. Your brain puts the pieces together and is able to perceive full vision without anything missing. This is why someone with age-related macular degeneration (ARMD), can be fooled into having a full visual field, but really may have a scotoma.
It is estimated that in 2012, there were 2 million cases of macular degeneration in people aged 50+ in the USA. That accounts for a 25% increase from the year 2000. By 2050, the NEI predicts that macular degeneration will hit 5 million and that means 6.3 million people will likely become legally blind!*
ARMD has two forms, the non-neovascular (dry ARMD) and neovascular (wet ARMD) form:
The dry ARMD is caused by the build-up of a metabolic retinal byproduct called drusen. Drusen is a yellow-whitish lipid protein substance that is created by the RPE layer and is deposited in Bruch’s membrane. This causes elevation of the RPE and can separate the sensory retina away from choriocapillaris. This disconnection causes numerous retinal problems and can result in blindness.
On the other hand, the wet ARMD is the formation of new blood vessels in the retina. This can occur between the RPE and Bruch’s membrane or between the retina and the RPE layer. Since the blood vessels are new, they tend to leak out and cause sub-RPE hemorrhages. However, while the layers are able to uptake and get rid of some of this blood, they can’t do it fast enough, resulting in scar tissue formation. If the body does not take up the leaky blood, further hemorrhaging can occur, which could lead to more serious problems such scar tissue build up in the retina. As scar tissue builds, a retinal detachment can occur occurs.
Unfortunately, there is no cure for this disease. There have been two federally funded studies called the Age-Related Eye Disease Study, or AREDS and AREDS II. These studies looked at the effect of nutritional intervention on patients with active ARMD. The newer study indicated that some antioxidants work better than others, thus incorporated lutein and xeanthin, which has resulted in a better formula in reducing the risk of ARMD. This study shows a resulting delay in the progression of ARMD, although not a complete stop to it.
There are also anti-VEGF injections available for the wet ARMD, which try and stop new leaky blood vessels from forming. Another treatment is a laser procedure, called photocoagulation, which is able to seal the leaky blood vessels. However, using this laser results in destruction of nearby retinal tissue. This actually creates holes in the patient’s vision, but it stops the leaking from occurring at that spot.
In conclusion, our amazing brain can actually fix most small scotomas through our complex visual processes. However, when the brain cannot “fill” in all the holes and patients come in with complaints of central vision loss, one possible diagnosis could be ARMD.