We eye docs have been sensitized to referring to changes in the macula as age-related macular degeneration, or AMD. It’s curious then that we persist in referring to age-related changes in the crystalline lens of the eye as “cataract”. It’s an old, antiquated term and many patients still conceive of it as some sort of growth that dims vision and has to be removed – as if it were a cancerous intrusion in a body part or system. I suggest that we would do better in gaining understanding on multiple levels by using the retinal analog, and referring to the condition as ALD.
A great article in the New York Times supports this notion. There are many implications in the effect of protein deposition in the lens, and how it alters incoming light. Increasingly we find that vision therapy populations in our practices are no longer just the young. How often do we consider the influence of early “cataract” development on the performance issues of adult patients other than changes in visual acuity or contrast sensitivity?
The notion of ALD is a more holistic one, particularly considering the influence of the lens in altering circadian rhythms. It has long intrigued me that the denaturing of the cyrstalline lens with age results in protein deposition of prions – the same beta amyloid protein buildup that occurs in the brain of Alzheimer’s patients. We are used to making the point that the composition and function of the retina qualifies it as brain tissue. The new way of looking at the crystalline lens suggests that it also participates in visual thinking.
As you read the article in the New York Times about the eye’s lens, all kinds of connections may spring to mind including the implications of color effects and the altering of light wavelengths on the retina’s SCN and circadian rhythms. This extends to considerations about the nature and effects of implanted IOLs for the treatment of ALD. Yet another reminder of the pervasive nature of vision.