Atropine and Myopia

I’m not going to even claim to know the entirety of the picture, but the current use and practice with it has been rather frustrating. Not because it’s recognition(or lack thereof) nor of anything related to its efficacy or lack thereof. I will state that the interesting factoids on atropine and myopia is when it simply does not work. Atropine’s failures can become the greatest strength in understanding myopia if the vision specialist would just look.

Fact 1: myopia is a vision problem, not merely refractive problem.

Fact 2: vision is not localized to the eyeball

Fact 3: Trolio et al study did not locally isolate vision to the eye ball as is often claim when one understands the known facts of vision(not eyesight).

Fact 4: vision involves many highly complex, not yet quantifiable, interactions of multiple sensory-motor processes between somatic, autonomic, subcortical, cognitive, non-cognitive, bottom-up and top-down neurological pathways.

Since we know that vision is not localized to the eyeball, neither should our study of myopia or any vision condition.

Every methodology of myopia intervention involves visual motion modifications—Ortho-K, Stellest Lens, MiSight and even atropine. Red light therapy too. For the optical interventions, too much emphasis is placed on where the light is focused rather than the optical experience, to which I’ll say the experience is utmost importance yet remains the chief blind spot. Change thr optics, change the experience. Change the experience, change the response.

However, if one’s habituated operation has “solidified” at a “motor memory” level, a mere change in optical experience would not be enough to sway the trajectory of myopia progression very much. This is my hypothesis in why optical interventions have an effectiveness rate of 50-70% only. Of course it’s better than nothing, but we need 90-100% and we should not be satisfied until we reach 100%.

Knowing also that sensory-motor arcs compose the visual experience and response, we can use this knowledge to better understand atropine at a different angle rather than searching for THE explanation from simply a biochemical one. I love the chemistry as I have a degree in Biochem, but we are complex living creatures and nothing would be so simple.

Autonomic sensory-motor arcs play a huge role in our vision. Any optometrist who has ever cyclo refractive has experienced this first-hand. Understand the sensory-motor arcs!

Enter Yerkes-Dodsons law. Although more of a lore than a law, it has not been ultimately disproven and has served as a good principle. We see this with the change in saccades and oculomotor responses during parasympathetic dominant activities such as reading vs an activity with more sympathetic involvement showing increases in oculomotor activity.

My hypothesis is that atropine interrupts the sensory-motor arc of the parasympathetic thereby preventing the autonomically driven downregulation of arousal/excitement.

However, autonomic adaptation should not be maintained for very long as other processes must proceed. I propose that the reason atropine fails to a certain degree is due to the interactions of other sensory-motor arc pathways, namely ones being developed at the motor-memory—parietal-cerebellar processing. It would then make sense that atropine would not have an effect on this pathway in particularly. The stronger these sensory motor arcs relative to the ANS sensory-motor arcs, the less effective atropine would be predicted to have.

This explains why some staunch readers never develop myopia while certain reading avoidants develop myopia anyway surpassing any parental myopia (some parents without myopia at all).

It also explains the data regarding increasing the dosage concentration of atropine improving effectiveness. The more solidified one sensory-motor arc is, the more intervention is required upon another.

The same would be true for red light. Rather than interrupt the sensory-motor arc at the ciliary body and uvea at both the muscular and proprioceptive sites locally, red light would interrupt this reflex-arc by feeding another sensory-motor arc that is antagonistic to arousal suppression via excitation.

However, why then should we use red light? We know THE best preventative factor—outdoor freeplay in the presence of sunshine which yields flavoring red and UV lights which enhance the antagonistic excitatory pathways. Yes, it’s not shown to be helpful after myopia is solidified, but did these studies account if those children wore their lenses or not during outdoor play? That’s an important factoid. Standard minus lenses decrease peripheral retina excitation and most lenses block a portion of UV. Which means there is a logical flaw in the study and therefore requires a follow-up repeat.

Schools need more recess and less downregulation of visual excitation and vision specialists should drive the demand for it. Parents should command from their schools.