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BLOG: Why are some cataracts wedge-shaped?
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In my clinic, the patients are typically in their 60s, 70s and 80s, the time of life when cataracts become more pronounced and start to necessitate surgery. Over the years, I’ve noticed some patterns in the types of cataracts I see, and I also started developing questions about why I see certain types of cataracts.
This article will attempt to dig a little deeper into these themes.
Why brown?
As the lens nucleus ages, brunescence can occur. But in the majority of cataracts, even in visually significant ones, this doesn’t occur in any large significance. The majority of nuclear sclerosis is a whitening of the reflected light, or white scatter. Of course, the denser a cataract is, the more likely it is to show brunescence. To answer the question of why some cataracts show a white scatter and some show brunescence, we must discover why any of this happens in the first place.
The causes for cataracts are varied, but the major two causes occur at the cellular level and the molecular level. The healthy lens is clear because the lens fibers are regularly and perfectly arranged, with a minimum of extracellular space (cellular level). Within those lens fibers, protein molecules are regularly and perfectly aligned so that there is minimal light scatter (molecular level).
To speak of nuclear sclerosis, we are speaking of light scatter at a molecular level, essentially a change in the proteins within each lens fiber. Light scatter occurs primarily three ways: these proteins clump together (spurred by changes in their cell membrane), forming microscopic aggregates and disrupting their formerly perfect molecular arrangement; water molecules force their way into the lens fibers, forming vacuoles large enough to see with the slit lamp; and the accumulation of an insoluble, yellowish pigment protein, which also forms microscopic protein, aggregates within each cell of each lens fiber.
The first two causes are responsible for a typical white-scatter cataract, and the last cause is how brunescence occurs. Whitish, nuclear sclerosis is the aggregation of pre-existing lens proteins or of water. Brunescence is the entry of a colored, pigment protein into a previously transparent lens fiber.
This brunescence not only causes light scatter – which, like regular nuclear sclerosis, reduces contrast sensitivity and visual acuity – but it also increases light absorption of certain wavelengths. If the density of the lens increases with age, and the proteins that fill it are mostly longer wavelengths like yellow, then shorter wavelengths like blue will be absorbed by the lens and fail to be perceived in the retina. A patient with brunescent cataracts will have a hard time perceiving blue, as Monet is thought to have had during his “Blue period” (Monet had to add more and more blue to his paintings for him to perceive even the smallest amount of the color).
Interestingly, there are many cultures with languages that do not have separate words for blue and green. These so-called “grue” languages seem to occur in geographic locations closer to the equator or in higher altitude than cultures with languages that have separate words for blue and green. The thought is that since these cultures have more UV-B exposure, perhaps they correspondingly have more difficulty perceiving the difference between subtle shades of short wavelength colors due to changes in their lenses. More on sunlight exposure later.
Why wedge-shaped?
Another question that comes up in clinic is why are cortical cataracts wedge-shaped? If the lens cortex encircles the nucleus 360 degrees, why are they often just one or two clock hours? Above we discussed nuclear sclerosis and changes in the lens at a molecular level, but cortical cataracts come about by changes at a cellular level. When I think of cortical cataracts, it helps me to think of the Y-sutures. You can search for a picture of how the lens fibers attach to the y-sutures, but essentially they leave a random site on the anterior Y, loop out to the equator of the lens and then loop to a random point on the posterior Y. As we age, new cortical fibers are laid down on top of old ones so that the newest fibers are the most superficial. But if you think about it, each fiber runs at most 180 degrees of the lens, and if you look at it from the equator of the lens to the Y-suture, each fiber looks just like a cortical spoke.
Cortical cataracts form from an insult to a single lens fiber, and this insult is often UV-B light exposure. The fiber becomes metabolically inactive, swells and then starts to degenerate. With this process, the fiber becomes opaque (for the same molecular reasons discussed above) and can also affect the adjacent lens fiber, thus creating the classic wedge-shape we identify with cortical cataracts. It also explains why cortical cataracts are most often inferior-nasally located. The inferior cortex is the most exposed to sunlight, and (depending on the size of the nose) the nasal side more exposed than the temporal side.
Incidentally, we can dig even deeper into the shape of certain cataracts. Cortical cataracts are wedge-shaped, but often solely anterior or posterior. This happens because the typical UV-B insult occurs to the older, deeper fibers and typically at the equator of the lens. The cataract then progresses centrally toward the closest Y-suture, which will be either the anterior or the posterior. It can then affect the neighboring fibers to its left or right but also to its anterior or posterior.
In a traumatic cataract the shape is often described as petalloid. This happens because the insult starts at the Y-suture and progresses outward/peripherally. It’s thought that the lens fibers are torn from their Y-suture due to the force of the trauma. Some kind of repair mechanism (still somewhat unknown) stops the cataractous fibers before they reach the periphery. In a lamellar cataract, the shape looks like a sand dollar. This occurs because some insult (most often metabolic problems such as hypocalcemia or galactosemia) causes opacification of an entire lens fiber shell, or the most recent “layer” of lens fibers put down.
Properly identifying the type of cataract for a patient is nice, but preventing or slowing the formation of cataracts is even better. Rather than a long lecture to my patients, I like to simply site evidence-based things he or she can do to lessen the chance of losing vision from cataracts. For instance, avoiding UV-B light and not smoking are two modifiable risk factors to help with cataracts. Also, multiple studies found less cataract formation in patients who use nonsteroidal anti-inflammatory drugs, beta-carotene, vitamin C, vitamin E, lutein and zeaxanthin.
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