The physiology of astigmatism reduction

So SPH reduction happens when pseudomyopia is relieved and active focus stimulates axial change. But how about the mechanism of action for CYL reduction?

(For simplicity’s sake, please assume regular corneal astigmatism, i.e., that the astigmatism is not due to an irregularity of the lens or eyeball, that the corneal axis and meridian are perpendicular to each other, and that the refraction varies smoothly between said axis and meridian.)

We know that simplistically speaking, when we reduce CYL (& correspondingly create the “spherical equivalent”), the received image, when inspected circularly, gradually cycles between undercorrection and overcorrection.

And the cornea is then supposed to reshape (by itself, with the assistance of the extraocular muscles, or however), thereby reducing the astigmatism.

But what exactly stimulates this to happen? Is the brain’s detection of the symmetry of the undercorrection vs. overcorrection (for astig reduction) analogous to active focus (for myopia reduction)?

With SPH reduction, blur adaptation (==> lack of active focus) is a real possibility that can hinder progress. Whereas for CYL reduction, is the corresponding adaptation to the over- and under-correction not an issue due to their cycling between each other (circularly across the visual field)?

Another question I’ve been wondering is, how does the reduction rate of astigmatism broadly compare with that of myopia?

I’ve tried to be clear and simple, but I do apologise if this posting is hard to parse.

Any insight or reference would be much appreciated!

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I’m not going to lie, but I feel astigmatism is a farce generally. Unless, like you say, the eyeball was literally born that way or they need it, like truly, I would skip it entirely. I would do the equivalent and then reduce -0.25 moving forward. This is my take!

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I am equally intrigued by the biomechanics of astigmatism reduction. What is happening when I am able to clear, for a short while, astigmatic doubling or trebling while doing monocular testing on the Snellen? If I do this for too long, I get a pain to the side of the nose, like sinusitis. This makes me think it is the extraocular muscles having to work very hard to ‘reshape’ the eyeball and then having to release, bringing back the astigmatic doubling. And what is happening when I do binocular testing on the Snellen with the same pair of glasses, and I see no astigmatic doubling? Are my oblique, mirror image axes of astigmatism in the eyes (50, 110) cancelling each other out, and how is that possible?

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I did some googling on astigmatism, and found this article
https://eyewiki.aao.org/Physiology_of_Astigmatism
This is way above my pay grade, although I did come away with the knowledge that astigmatism is not a simple issue, can fluctuate during the day and during a lifetime and is not just a matter of extraocular muscles. But that does not help those of us wanting to know what mechanisms lead to its reduction or elimination, which seems to have been proven possible by many Endmyopiers.

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I wont bother trying to dive into the theoretical, but as someone with an eye starting at -2.00sph/-4.25cyl, my sph is moving proportionally faster than cyl. My current ideal prescription for that eye is -1.25sph/-3.50cyl. I’m not sure what to think because the rate of both seem the same, but we know cyl and sph are “weighed” differently in some endmyopia adjustments with a 2:1 ratio. Also there’s the diminishing returns we get as we are closer to zero, so my tendency is to say that cyl is still slower.

If we use the ratio to level the playing field (multiply sph by 2), my starting point would be something like -4.00sph/-4.25cyl and my end point would be -2.50sph/-3.50cyl. So sph would still be faster.

I’m one of those football-eyed freakbabies though, so your mileage may vary.