A few thoughts about astigmatism from the point of view of a medical student

Hello everyone!

I’m a medical student and I want to share with everyone the knowledge I have acquired about astigmatism by reading pretty much every post from endmyopia about it and also by learning the mainstream medical point of view and asking doctors questions in my 2 weeks long ophthalmology rotation. One reason I’m doing this is because lately I’ve seen a lot of posts here and on the facebook group about astigmatism and a lot of people are asking questions about reducing it, spherical equivalent and so on. Hope you’ll find the information useful, I acknowledge my humane limitations and I’m open to discussions.

1. What exactly is astigmatism? - Basically, astigmatism happens when the cornea is not perfectly shaped (like a sphere), but resembles a rugby ball. That is, the length of the horizontal and vertical axes are different, thus the refractive power of the lens (cornea) varies. I don’t want to get into a lot of details, but what this means, is that there are 2 images formed on the retina because of the difference in refractive power along the 2 axes of the cornea. 2 images mean what we on endmyopia call astigmatic blur.

2. What does the axis number mean? - It is the angle (that’s why it’s written in degrees) between the two principal axes of the cornea that are different. This can be anywhere between 0 and 180 and the 2 different images formed on the retina are misaligned on this particular direction.

3. Why is astigmatism corrected with cylindrical lenses? - To correct myopia we use spherical lenses that diverge the all the rays of light, thus moving the image further back in your eye. To correct astigmatism, we use cylindrical lenses that diverge the rays of light only on a certain axis. Not gonna go further into high school physics about lenses.

4. Are there different types of astigmatism? - Yes, I’m not gonna go into all the types, but you should (understand at least) know what’s the basis of defining different types. You have 2 images formed and one retina in one eye. One image can be formed either in front of the retina, on the retina, or behind it. The other image - the same. By playing with different possibilities, you can have different combinations, so different types of astigmatism. I will exemplify just 2 types:

a) Simple myopic astigmatism is when one image is on the retina and the other is in front of the retina. You need a cylindrical correction that moves that image back on the retina.

b) Compound myopic astigmatism is when both images are formed in front of the retina, but not in the same place (that would basically mean myopia). You need both spherical correction (that moves both images back, one being on the retina now) and cylindrical correction (that moves the other image further back, aligning them both on the retina taDA! the sharp image is formed)
Most of endmyopia users that also suffer from astigmatism probably have this type :slight_smile:

*Astigmatism can also be classified based on the axes number, but I don’t feel like going into these details now. Try wiki. *

5. What is spherical equivalent? - Giving you some numbers because it’s easier to understand. Let’s say you have (talking only one eye for the sake of simplicity) -2 spherical and -1 cylindrical (with axis y). You have one image that is formed in front of the retina and you need 2 diopters to move it back. Second image - you need 3 diopters to move it back, 2 are from the spherical lens and 1 additional is from the cylindrical on the y axis. Spherical equivalent means something in between that, let’s assume is -2.5 spherical that moves both images back at the same time, but not putting any of them on the retina. Think of this like a compromise that cannot work perfectly because neither image is where it should be.

6. Why does Jake says you don’t need correction for astigmatism when it’s under a certain value (0.5-1.0) ? Because it’s not that much :slight_smile: and if you can see fine without it, there’s no need to use it.

7. What can cause astigmatism? - Medically speaking, the exact cause of astigmatism is unknown. The eye is a VERY VERY VERY sensitive and delicate organ (a third of a millimeter of misalignment between the image that is formed on the retina and the retina equals to 1 dioptre of myopia) and just small inaccuracies in the lens of the eye that can arise from unknown factors (genetics for example) can cause problems. Mainly, the cornea is affected in some way that makes it irregular (picture the rugby ball again).

8. Then is there such a thing like lens induced astigmatism from progressive myopia? - Yes and No. I don’t have a definite answer to this. Intuitively, when the eye is very big (high myopia) there is the possibility that it didn’t enlarge uniformly, thus making it astigmatic.

9. Why does Jake say that genetic astigmatism is rare? - It’s not that rare. According to wiki, 30-60% of adults in Europe and Asia have astigmatism. There is a rare disease called Keratoconus and it’s caused by a very nasty shaped cornea that gives progressive and very high astigmatism. This is pretty rare, but low genetic astigmatism can occur with higher frequency than Keratoconus.

10. How do I know that my astigmatism is from my cornea? - You go to a ophthalmologist that will look at your eyes with a refractometer AFTER he put cycloplegic drops in your eyes, eliminating cilliary spasm and thus any accomodation reflex that might occur during the measurement. On the piece of paper that comes out from the machine, it should be written (if you have astigmatism) how much is from the cornea, also giving you other numbers for nerds. The measurement of the the topography (how it looks) of the cornea is called Keratometry (it measures your cornea).

11. Why is astigmatism so frequent? I’m so sad to hear so many people have astigmatism :frowning: - Actually, there is something called Physiologic astigmatism. This means that is normal. Wait, what?! Yes, a lot of people have slight astigmatism and they usually don’t need correction (because it’s very low). It is caused by the weight of the lids that press unequally on the cornea every time you blink, thus changing the shape of it just a little (VERY little actually). This would be another argument for point 6.

12. Is astigmatism caused by uneven cilliary spasm or imbalance between the muscles that move the eye? - I HIGHLY doubt it, but think for yourself. This is my opinion based on my anatomy knowledge.

13. Enough with the talking, can I reverse my astigmatism? - If we assume that you can reverse myopia by changing back the eye to it’s normal size (through AF, positive stimulus, outdoor time, bifocal planes etc), we could also assume that you can reverse back the astigmatism that was created during the elongation of the eye. If you have low myopia, and higher astigmatism (that you can pinpoint through keratometry to an asymmetric cornea), my feeling is that you might not be able to see clearly without changing the shape of your cornea somehow.


To sum things up (because this post has gotten way bigger than I expected), astigmatism is usually caused by a different shape of the cornea (we don’t know why this happens) that forms 2 different images on the retina. There are a lot of types of astigmatism. If you have less than 0.75 it’s probably physiologic and you should wear cylindrical correction only if it bothers you that much.

P.S. What I’ve written above is my personal knowledge about astigmatism and I thought that by sharing it with you, you’ll gain something from it. This is by no means medical advice! I don’t want to hurt anybody’s feelings with my opinions that might be different than what others think. I’m aware that what I think I know might be wrong. I’m open to discussions and I’l respond the best I can and when I have the time. Feel free to leave a comment and tell me what you think! Have a lovely weekend :slight_smile:


Hi @lona26,
First of all I’m impressed! Thank you for sharing this. Have to reread it but it is very insightful!


Could you elaborate on the part about the extraocular muscles?

On Rhesus monkeys, corneal astigmatism can be lens-induced (click for a study). I’m not quite sure what mechanism other than the extraocular muscles could even do this. The cornea shouldn’t be able to detect uneven defocus, let alone react to it.

I find this idea, and in particular Forrest’s functional theory of astigmatism, quite convincing, and couldn’t find anyone who has shown evidence against it. Why would you say it is anatomically implausible? Intuitively, I’d think that if two opposing extraocular muscles pulled at the same time, while the others stay relaxed, it seems like this could cause corneal astigmatism.


Thanks for the links! I have to admit I wasn’t aware of Forrest’s functional astigmatism theory. It’s pretty interesting, I just skimmed both articles, but I want to read them thoroughly when I have some time on my hands.

@Varakari The main reason why I said extraocular muscles can’t cause astigmatism is that the point of insertion (that is the place on the eye ball where the muscle attaches) is a few good millimeters away from the place where the cornea ends and the sclera (white part of the eye ball starts) starts. Given this distance, I think it’s highly improbable that the cornea can be affected in any way by the traction applied on the eye ball by the muscles.

The cornea is a very, very sensitive part of the eye. It’s so badass and amazing, that we cannot artificially create a lens that is so thin, yet with such a high refractive power (~40 diopters). The only way to replace it, it’s to take it from a donor. My point is, the cornea being so sensitive, I don’t think “evolution” would put it in a position to get deformed by the mere movement of the eye ball. When one muscle pulls to hard, you get strabismus and this is a different condition. Doctors can perform surgery and reinsert the muscle to correct for it, but the condition itself has nothing to do with astigmatism.

Anyway, if you want further information, you could study the embriology of the eye, to better understand the relation between different parts of the eye and how they interact with each other when they develop. Hope I answered your question!


If I remember my days in medschool correctly, the sclera is a continuation of the cornea with a few differences being that at the limbus, some corneal layers disappear and the collagen fibrils change size and alignment so that their mesh-work in the sclera diffuses the light rays instead of passing them through like in the cornea.

Collagen being a continuous and primary structural component of the cornea and the outer layer of the sclera, leads me to believe that the traction on the sclera by the EOM may have an impact on the shape of the cornea.

The methodology of Forrest’s study is not perfect, as he himself has stated in there, along with suggestions for future researchers how to fix it, but his conclusions definitely warrant further research on this theory, and in my personal opinion, it wouldn’t hurt to try to apply his therapeutic exercises to oneself, if one has regular astigmatism.


Thank you this is what I have been looking for. It’s still a little complex for me but I will re-read it. Better than anything else on the web about astigmatism! - Mery

If astigmatism can be induced by lenses, shouldn’t it be possible to intentionally induce it in order to equal out corneal astigmatism? I was thinking about this, since I struggle a lot with cyl reductions in my prescription (I had cyl correction before sph, so probably not lens-induced), but I’m not ready to give up yet. Any thoughts/theories on this? :smiley:

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I also had same funny thought while looking at my old prescriptions. What I found out from my last 10 years prescription that RE always had axis 180 with different Cyl values, but my LE was axis 180 in some prescription and 90 in others. Well, since at that time I didn’t pay much attention, just got prescription and glasses.

Before buying my first glasses after finding EM, I went to opto and checked. It seems that LE did not have any CYL, only RE had, which was higher than previous values. I got doubt whether CYL with diff. axes removed astigmatism in LE or it never had initially!!

Thanks for summarizing astigmatism information. I have hard time understanding it properly. Will have your info printed out to refer when I feel confused again.

Fascinating thread! This is a medical explanation of the cornea’s role in astigmatism, and matches my growing theory that myopia (and hyperopia) is possibly mostly a cornea change.

Never did understand how it could be elongation of the eye, a spherical eyeball can turn easily in a spherical eye socket, but it just didn’t seem plausible that a stretched eyeball would rotate easily.

It also suggests that what we call “ciliary spasm” might just be temporary cornea deformation induced by the ciliary squeezing the front opening of the eye closed for a while, just like those old hard contacts could temporarily “correct” myopia by reshaping the cornea and the cornea would hold that shape for a bit after cornea removal.

I’ll write this up better when I have time.

Now I’m off to see if my eye’s astigmatism changes when looking hard to the side …

Ha! It worked! My left eye has 0.25D of astigmatism (the right has none). However, I was able to change it!

This post is useful as it’s how I’m spotting astigmatism in my eye:

Looking straight ahead with the right chart and my left eye, I have sharp lines on the lights tilted just to the left of vertical at the blur horizon.

When I look to the left and push it (e.g. trying to look beyond where my eye can go, which causes my left rotator muscle to pull continuously), the astigmatism clears! (no dominant sharp lines). Going the other way is hard due to the nose blocking the view :slight_smile:

So that was cool, it suggests the rotator muscles can indeed change the shape of the cornea. If so, imagine what would happen if all 4 muscles pulled at the same time, could that be active focus?

If so, then that could explain why active focus could both recalibrate spherical as well as cylindrical, if it puts stress on the cornea which over time reshapes it, and if the cornea is the primary instigator of myopia/hyperopia.

What if myopia is primarily cornea shape change and not actually shortening/lengthening of the eyeball?

I’ve always wondered how they measure eye “length”. If it’s sound based (e.g. ultrasound), wouldn’t that be affected by cornea thickness/properties? If those changed during myopia progression/reversal, could that affect the readings?

I’ve also always been bothered by the elongation theory. A spherical eyeball in a spherical eyesocket can easily rotate. An elongated eyeball in the same eyesocket should have difficulty rotating, and deform when it does. But when I wore contacts, the view was the same no matter which way I looked. So how could my eye be elongated?

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Not to mention the eyeball can bulge out forward of the eye socket.

Makes perfect sense to me, really.

Yeah bulging forward makes sense. Still, I’m becoming more and more convinced that the cornea plays a big role in the eye’s calibration.

I believe that myopia is elongation of the eyeball, not sure why you are throwing this accepted explanation away. Everyone subscribes to this explanation : optometry and Jake as well. Astigmatism is of course corneal as you say, they are two different things, so I accept what you’re saying for astigmatism but not for myopia

It is accepted amongst most of society and medical profession that myopia is irreversible, yet here we are :slight_smile:

Anyway this is just my current theory, and the only theory I have so far that explains everything, from how myopia/astigmatism occurs, how reversal of both works, etc. The elongation theory has never been explained how it happens and what mechanism triggers it, nor why it should ever shrink. The cornea theory has direct cause (deformation of the cornea due to stresses/strains caused by muscle action) and fits all the scenarios (why orthok works, why ciliary “spasm” works, why my eyes stay “better” for a while when I cease AF)

So I like it because it fits the evidence better and doesn’t require hand-wavy “ciliary spasm causes magic elongation for some reason” which was always bothered me.

Excellent! I’ll have to throw in my experience from my last official prescription. I had 2D and 0.5 and 1.0 cyl added to my old blurry prescription, which was quite a lot. It made the optician uncomfy giving it to me clicking that machine 4-6 times. Then weeks after in a bus (thankfully), I felt my eyeball squeezing all of a sudden in the front of the eye more like top down. I’ve never felt the squeezing happening that strongly, because the increments are usually small. Only the muscles could’ve done that so fast, and they may very well pull the cornea since its a continuation of the sclera and its connected together. Maybe that’s why they don’t give you much diopters at a time, so you never feel what’s happening. Needless to say what happened with my 1st normalized reduction.

Vision facts are: 80% cornea, 10% lens and 10% jelly inside the eye gives you your vision. Where’s the axial length from these facts? I recall Bates saying that he doesn’t trust any machines in the industry, because he knows they’re only made to make money. And that the machines only measure this and that but not relevant stuff.

One thing remains the same, and that is eye exercises hurt, axial elongation or corneal shaping. I tried moving my eyes to put some blood in the muscles and the inner eye started to hurt after repeated days of eye drills from youtube. So, how would that cornea be reshaped then without actual movements?

First off, if you’re doing something that hurts, stop it! :slight_smile: Eye change (at least in the myopia direction, and now in the other direction) never hurt me, the main thing is eye fatigue (first after hours of ciliary spasm, now after hours of AF).

Secondly, the cornea can be reshaped by stress/strains due to muscles. The ciliary muscle constricts your pupil area opening, which the cornea is attached to. That’s how it reshapes the lens, the cornea is attached, so it must be affected too (in fact, it might be a major part of accommodation). My pet theory is the rotator muscles, all pulling at once, has the opposite effect.

The pulling the edge of the eyelids (pull on the side of the eye where the two lids meet) distorts the cornea, and shows not much force is actually needed to change your vision. Using this technique, I can correct my myopia temporarily on one axis (zero Sph, massive Cyl). How is this possible? Eyelids pushing on the cornea changing it’s shape. Obviously it snaps back. But what happens to the cornea with stress from the ciliary or rotator muscles over years?

Just wondering how your theory stacks up against the empirical data collected by @Varakari using the machine that measures axial length and shows it decreasing year over year?

Good question, I’m curious how that machine works? How would changing cornea thickness/shape affect the readings?