Motion as the Hidden Thread: Rethinking Myopia, Binocular Vision, and Why We’ve All Been Measuring the Wrong Thing

I’ll respond to the following article: https://reviewofmm.com/is-treatment-needed-for-accommodative-convergence-issues-before-myopia-control/

Why myopia control folks and binocular rehab nerds keep talking past each other, and how the real answer’s hiding in something docs actually measure or prove for—visual motion response.

Let’s start with history nobody quotes. Back in

the 1930’s and 1940’s, optometrists grinding on strabismus, amblyopia, convergence hiccups, and learning messes already obsessed over myopia. It wasn’t some TikTok trend; vision therapy baked it in. Yet today you’ve got primary-care champs proclaiming “add power doesn’t slow myopia,” while behavioral-optometry dinosaurs nod sagely and say, “keep talking, pal.” Same patients, opposite scripts. That’s the grand disconnect.

The culprits? Two things: what we test, and what we blame. Recent reviews—slick tables, big sample sizes—scan AC/A ratios, lag of accommodation, lead of accommodation, relative accommodation, the works.

Verdict: “No difference between kids who myopiate and kids who coast.” Translation: those numbers are tombstones, not trailheads. They show endpoints, not why the car went off the road.

Cue my undergrad flashbacks. Health-psych professor: “Falling asleep with shoes on equals morning headache.” Duh, booze was the driver. Gen-psych professor: “Ice-cream sales spike with murders—summer heat’s the shared dad.” Correlation isn’t causation; it’s homework. So between myopia and wonky binocularity, what’s the shared dad? Simple: visual motion/visuospatial processing and response.

I check it every day with OKN strips—monocular, binocular, left, right, sometimes up-down. Children with hyperopia plus reading pain, adults post-concussion, you name it—many display deficits in visual motion processing of some form. Same glitch shows up in ortho-K patients who flatten, MiSight wearers who stall, even the random six-year-old in +0.25 who stops inching up a diopter a year. Motion deficit. Motion fix.

Now watch this: peripheral hyperopic defocus isn’t magic; it’s a fancy form-deprivation hack that chokes the peripheral retina’s motion detector. Primary Care Myopia-control peeps chant “hyperopic defocus,” but peel the label off and it’s still motion. Plain old form deprivation works too—ask any chicken, rabbit, or mouse, or other little critter that was involuntarily subjected to experimentation. The lens shape doesn’t matter; the motion bump does.

Flip side: slap a minus on—boom, motion stalls in the periphery, eye keeps stretching. Its physiology 101: Positive feedback loops want steady motion; negative loops solidify stasis. Myopia? That’s the runaway loop when motion stalls and emmetropization adaptation unwittingly fails.

Here’s where it gets cheeky. Individualize an Add +0.25, +0.50, or even +0.62 at near—primary-care crowd says “won’t touch myopia.” Vision therapy crew slips it in anyway and swears progress slows. Who’s right? Both, if you “zoom out.” That tiny plus isn’t taming central accommodation; it’s juicing peripheral motion. Ever see nystagmus melt with +0.5? Not because the kid’s lens flexed—it’s because motion feedback looped back quieter. Depth-of-focus absorbs the accommodative nudge; motion eats over-emmetropiation.

Suppression’s the same story. Keynote optometric speaker calls it “down-regulated visual motion.” Give me ten minutes with a rotating drum, toss in vestibular input, suppression flips off like a bad habit.

No surgery, no patching—just motion.

So what do we do? Burn the AC/A charts. Run the full 21-point adaptation battery: Multiple

Dynamic Rets, OKN functions, fixation-disparity adaptation—not just static disparity—visual-motion thresholds, pursuit gain, saccade latency, the kitchen sink. Track how the system self-tunes, not where it lands.

Side note: I ran this on myself—n=1, total mad scientist. Twelve years ago at minus -6.50, certified myope. I’ve crawled into -5’s, then -4’s—without atropine, without night lenses. Am I shrinking my eyeball? Who knows. Am I recalibrating motion-driven perception? You bet. Proof? TBD, but the blur chart doesn’t lie. I’m now able to crack out 20/15 with a -2.25 MiSight lens.

Bottom line: stop arguing if binoc disorders cause myopia or myopia causes binoc disorders. They’re twin symptoms of one engine rattle—motion processing gone lazy. Treat the engine, not the smoke. Ortho-K, MiSight, low-dose plus or atropine—they all crank the volume on peripheral motion. Figure out how each kid’s brain samples that motion, then coach it. Everything else is just optometry theater.