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What Happened to the Trap King's Eye?

By Laureano Andrade Vicenty 6/4/2016

     Fetty Wap's eye has gather much interest during his rise to fame. Fetty wap has been recorded saying that he lost his eye as a child to glaucoma. Below is that video. Today, we will discuss the anatomy of the eye, and what goes wrong with it with the condition of glaucoma.

Structure and Function of the Eye

     The human eye's major components is the cornea, which is the clear covering of the eye over the hole that is the pupil. This cornea, a lesser known fact, actually functions to bend light significantly, acting as a lens, although not named as such. The pupil is surrounded by the colored part of the eye, the iris), the lens, which finely bends light to focus it on the retina, and then goes through a few retinal cells that send that information through the optic nerve up to the brain. However, what also should be considered is the fluids that fill the eye, namely the aqueous and vitreous humor. The names, for our purposes, isn't really important, but what is important, is to recognize that the eye is filled with a fluid. We will focus on the aqueous humor. If there is fluid in the eye, it is reasonable to think that there is an inlet and an outlet for that fluid, which brings us to the ciliary bodies and the canal of schlemm. The ciliary bodies synthesize and secrete the aqueous humor, and the canal of schlemm is the exit site for this fluid. Glaucoma results when this outlet is blocked, or when the rate of fluid secretion is much greater than the fluid flow outward. This increase in IOP is correlated with nerve damage, and if left untreated, vision loss results.


laughing man

There are many types of pressure, but pressure is really force per unit area. Fluid pressure results from fluid molecules colliding into the walls of a container. This is best visualized with a balloon. As a balloon is heated up, or you add more air (which is a "fluid" in physics), the number and frequency of collisions increases, eventually resulting in a pressure so great it overcomes the elasticity of the balloon and goes POP! Thankfully, this does not happen in glaucoma.

Anatomy of the eye

How can one go "partially" blind?

While glaucoma may come in many forms, it can be most generally understood as a condition characterized by an elevated intraocular pressure (IOP) and subsequent optic nerve damage, although the characterization of requiring elevated IOP for glaucoma is beginning to change (Scuderi et al, 2015) (Gupta et al, 2009) . The elevated intraocular (intra-inside, ocular-eye( pressure is usually associated the blocking of the fluid outlet, the canal of schlemm. What does that actually mean? It means that there is an increased amount of molecules colliding into the container of the aqueous humor in the eye; there is simply too much fluid (see the sidebar to better understand pressure). The molecular details that lead to optic nerve damage is not clear, but the increase intraocular pressure certainly is not the causal factor, and what leads to nerve damage appears to be multifactorial (Gupta et al, 2009). So I am not going to go there, however, I can tell you what the "optic nerve" is. The optic nerve is a collection of linear projections of neural cells (axons), and serves as the conduction pathway, much like an electric circuit, for visual information that has been transduced from light into electricity, and that current hits the optic nerve, it heads towards the visual association areas of the brain (occipital cortex). The fact that it is a collection of cells, rather than a singular cell, tells you that you can have damage to the optic nerve without complete loss of function. With that said, as a generalization, nerve cells DO NOT REGENERATE. This is the biggest problem with glaucoma, if it is not caught early, the damage is irreversible. This irreversibility, you now understand, is due to the fact that nervous tissue does not regenerate. Further, you should now understand why it is not simply an "all or nothing" event with respect to blindness, but rather a matter of degree, and this is because the optic nerve is not one cell, but rather many outpouchings of cells coalescing to form the so-called optic nerve, hence you can damage some cells, while leaving others intact. In the next section we will discuss one treatment for glaucoma, which is the famed maryjane.

Why marijuana to treat glaucoma?

popeye with ganja

     The idea, when treating glaucoma, is to lower the pressure within the eye. From what I told you in paragraph one, you could begin to guess what those areˇKwidening the canal of schlemm, decreasing the secretion of fluid from the ciliary bodies, etc. All of this is directed at lowering intraocular pressure. The devil's cabbage runs a similar scheme. Marijuana is a cannabinoid, and its molecular structure mimics naturally occurring molecules called endocannabinoids in the body (Mackie, 2008). When binding to the proper receptors in eye cells, of the diverse set of pathways activated, one leads to the decrease in intraocular pressure. However, the effect is not very long lasting (~3hrs), and isn't really a feasible treatment method, as you would be having to smoke every four hours or so. Not to mention, I for one would not want to be high for the entire day, but I supposed I could imagine someone who would. Take away: Glaucoma is generally characterized by an increase in intraocular pressure, and if not caught early, while the mechanism is unclear, can lead to extensive optic nerve damage, and hence partial or full blindness.


Gupta, S., Agarwal, P., Saxena, R., Agrawal, S., & Agarwal, R. (2009). Current concepts in the pathophysiology of glaucoma. Indian J Ophthalmol, 57(4), 257. doi:10.4103/0301-4738.53049

Mackie, K. (2008). Cannabinoid receptors: Where they are and what they do. J Neuroendocrinol, 20(s1), 10-14. doi:10.1111/j.1365-2826.2008.01671.x

Scuderi, G., Iacovello, D., Pranno, F., Plateroti, P., & Scuderi, L. (2015). Pediatric Glaucoma: A Literature's Review and Analysis of Surgical Results. Biomed Research International, 20151-8 8p. doi:10.1155/2015/393670