Observations from having my pupils dialated

Yesterday I had my follow up eye exam. Late last year I had a “blind spot” appear in my vision, that turned out to be a cotton-ball spot inducing a floater. Yesterday was the follow up, and long story short, the eyes are fine (the spot is gone, and no new ones).

To check my eyes, both times my eyes were dilated. The drops they use paralyze the iris muscles, and as it turns out, also paralyze the ciliary muscles. The first time I didn’t know this, and only found out when I was unable to focus close at all. What surprised me most, was my active focus range was totally unaffected, indicating to me that my version of Active focus does not involve the front of the eye.

This time, I came prepared. I wanted to see what accommodation range I had while the front of my eye was paralyzed. What I found surprised me. Once again, active focus was unaffected. Sure enough, nearer accommodation was (mostly) inhibited. However, when I tried to close focus (vs let it happen "naturally), I found I could indeed get a little accommodation (about 1 diopter, according to the Meow-Sure app). More importantly, however, the slight sensation on my eye when it finally kicked in was similar to active focus, and different than normal close accommodation.

This led me to a theory I have now that finally answers several nagging questions, mostly around why some people get myopic and others don’t (for similar levels of close-up). What I realized, is that that 1D of “extra” accommodation is likely my oblique eye muscles acting as an antagonistic pair. Since they’re balanced, my eye doesn’t rotate, but acts like a ring around the eye, squashing the “equator” and thus lengthening the eye (causing the “accommodation”. Think about taking a water balloon, wrapping your fingers around the middle like a ring, then squeezing, what happens to the balloon’s ends? Active focus, from my guess, is the rectus muscles all pulling on the eye, squashing it along its axis, yielding a little more distance focus, kind of like holding a balloon on your belly, and pulling on the edges of it towards your belly (the balloon flattens a bit).

It is my personal belief these two forms of accommodation drive eyeball shape size over time. Extended oblique use squashes the eyeball leading to eyeball lengthening (we call this progressive myopia). Extended rectus use squashes the eyeball in the other way leading to eyeball shortening (we call this progressive hyperopia, and I believe use it to undo myopia).

So, given this wacky idea, how does it explain why some get myopia and others don’t? Well, extended closeup with just the ciliary muscle leads to ciliary muscle fatigue, which means you no longer can focus that close (until your ciliary muscles get some rest). Those of us who “figure out” how to use the obliques to get extra accommodation use that and keep doing close-up for longer. Those who don’t will likely go do something else. By figuring out how to get an extra “kick” from the obliques, many of us extend near focus time dramatically. Why can us myopics do close-up for hours, while our “perfect vision” friends cannot (they get tired of it after a while)? However, the downside is over time the eyeball squashing leads to eyeball changes and thus myopia. Our 20/20 friends never figured this “trick” out and thus only use ciliary muscles to accommodate, and never got on the myopia conveyer belt.

I have no idea if this is right or not. But finally I have a working theory that explains everything (why myopia occurs, why we can reverse it, why some never get near-sighted, and how that all works). And it’s backed up by my experience of having my eye front (iris and ciliary) paralyzed, yet still able to accommodate both plus and minus a bit. It even explains why those who get cataract surgery sometimes can still accommodate close up a bit despite rigid pupils that are no longer affected by the ciliary muscle (they might do it by obliques squishing the eyeball causing the retina to move back from the lens).

And that’s cool, finally a mental model on the eye’s behavior that addresses pretty much all the mysteries I’ve had about it :slight_smile:

Now, someone please shoot down my ideas for me :slight_smile: :slight_smile: :slight_smile:


So as a practical advice we could say that close-up maybe not a problem until you feel your eyes get tired. But as soon as you feel that, you should just get up as soon as possible.


Super interesting. I enjoyed reading your hypothesis. I’m open to it unless someone else has a good reason to debunk it.

I am not convinced on your hypothesis though of why some people get myopia and others don’t. You have suggested:

Why can us myopics do close-up for hours, while our “perfect vision” friends cannot (they get tired of it after a while)?

That’s the frustrating thing though - some of our “perfect vision” friends have equal or worse habits to us. It isn’t a simple, balanced equation. If only it were! I think this is where there is space for genetics - how talented our lovely little eyes are are making those changes, how accommodating they are. So not that genetics is the reason for myopia, but that it influences how eager our eyes are to respond to stimulus.


I think you’re right or at least on the right track. Dr Bates was a surgeon and he claims to have seen many patients who could still accommodate with their cilliary muscle paralyzed or cut.

In Lasik circles the doctors point out that the shape of the eyeball changes measurably (0.2D) just from looking down and reading for half an hour, and that simply lying on your back waiting for them to perform surgery can change the shape of your eyeball .11D or more, which can mess up their surgery because they’ve measured you while seated and they operate on you lying down. They’ve got the equipment to measure these things accurately.

So I agree with your water balloon analogy. Maybe the eye is stiffer than a water-balloon, but it’s a physical object and gravity and muscles are all going to deform it when they pull on it in various directions. Stuff like the tear film on the eye provides another 0.1D of diffraction, eyelid pressure can be 0.4D, the eyeball isn’t made of stone or floating in a vacuum. CRT or Ortho K contact lenses can deform the shape of the eye overnight enough to dramatically effect vision. The cilliary muscle may do the “heavy lifting” of accommodation for most people, but all the other facial muscles and things attached to the eye have got to be able to “put some English on the ball” too.

1D of refraction is associated with .25 to .5mm of axial elongation, so in the “squishing the water balloon” scenario the deformation of the eyeball only has to move it a quarter millimetre to squeeze out an extra diopter of accommodation. That’s only 1% of the eyeball’s total length, so not a great big deformation.

It’s one of those things like wiggling your nose your your ears. Some people have figured out how to do it and can do it readily. You only need to be able to squish or stretch the eyeball a little bit to get another diopter or two beyond whatever the cilliary muscle alone is capable of.

Probably the fluid in the eye sloshes around a little bit too when you make rapid eye movements or shake your head, to see something you don’t necessarily have to have it in proper focus for more than a split second, just long enough that your brain can figure out what you’re looking at. Blinking probably deforms the eye for a moment (changing its shape) in addition to re-distributing the tear layer.

Edit: Another thought is that to the extent that your eye isn’t “perfectly shaped” you can probably take advantage of the little glitches and irregularities (such as “functional astigmatism”) and tilt your head a little to an angle and find some spot in one of the eyeballs you can see through that gives you better focus. Since it’s not a perfect sphere you should be able to move your eyes and head a little bit to find some spot on the eye that can focus on what you want to see (like using a mutifocal lens).


An interesting read! :slightly_smiling_face: Though there are some bits I hope you can clarify for me:

Does this mean Active Focus for distance vision does not require any activity from the ciliary muscles? I was under the impression that ciliary muscles kind of get stuck and we un-stuck with the help of Active Focus. Therefore I am surprised that “prevention of any movement” (ie paralysis) can still produce Active Focus results.

Pardon me for being clueless but do we assume that the paralysis make the ciliary muscles achieve a relaxed state? And therefore is the reason why Active Focus still works during ciliary muscles in paralysis?

Nobody inc. Jake ever said that genetics isn’t a part. They say genetics is the potential to get myopia but you still need the bad stimulus of prolonged close up

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I’m pretty sure that what we call with the umbrella term “Active Focus” is at least 2 or 3 different mechanism.

That’s true, but most likely not in the sense you mean. So you have a stuck ciliary muscle. You do Active Focus which somehow happens not directly with the ciliary, but which results in a relaxed ciliary too.


I know. Hence why I was adding it in to Hoofjr’s hypothesis.

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