Use Atropine for Myopia
I recently read “Myopia Regulation: Myth or Megatrend,” by Drs. Legerton and Chou (August 2009). I applaud them for acknowledging the significance of myopia as a world health problem and that it is the seventh leading cause of blindness with associated risk of cataract, retinal degeneration, retinal holes/detachment, choroidal neovascularization, etc. Drs. Legerton and Chou suggest that the loss of vision is even more important than many other diseases (e.g. diabetic retinopathy or age-related macular degeneration) since myopia affects patients earlier in life. Keeping these leading statements in mind, Drs. Legerton and Chou failed to understand the significance of two important treatments of myopia.
Though the COMET study found only small statistical differences in the use of bifocals or progressive lenses in slowing myopia progression in the first year, subsequent papers by the same authors have found progressive lenses to have a positive effect in controlling myopic progression in two subsets of patients. Patients with esophoria and patients whose parents also are myopic.1,2 Because the risk of progressive lenses is only the cost of the lenses, it might be prudent to prescribe progressives in these two sub-groups.
More glaring is the faulty application of basic research and clinical trials concerning the interpretation of atropine studies. Every animal and human study, since 1965, well performed or not has come to the same conclusion that atropine is an effective medication in slowing down the progression of myopia.3-25 The mean rate of progression of patients with myopia is 0.50D per year, while patients on atropine had progression rate of approximately 0.05D; a ten-fold decrease. Stated another way, a 1.00D myope at age 6 without treatment would most likely become a 6.00D myope by 16 years of age, while a patient on atropine would most likely become a 1.50D myope.
The authors point out that although atropine is successful in slowing myopia, and it has no reported serious side effects and that it is not the standard of care. In fact, it probably should be! The major obstacle blocking atropine’s universal acceptance is the lack of a major pharmaceutical company doing due diligence to get FDA acceptance of atropine. The reason for this logical: there is no financial incentive. Since atropine has generic status, no pharmaceutical company has an incentive to perform the clinical trials necessary to obtain market approval, and then market it like Restasis. Thus, the lack of standard of care is more likely financial in nature than clinical.
The authors suggest that loss of accommodation and dilation associated with atropine might affect academic and sports success, make the patient more sensitive to sunlight, or create mydriasis that would be socially unacceptable. They offer no scientific support for these conclusions. As a matter of fact, most of the studies report a low dropout rate for patients prescribed atropine and that the level of complaints is fairly low. Patient acceptance is high in all the studies performed to date.
I presume by the tone of the article that neither author has prescribed atropine to their patients or even offered it as a treatment option when patients ask, “Is there anything I can do to slow down the progression of my myopia?” The answer should be “yes.” The patient should be advised, “You can be prescribed a drop called atropine, which has been shown to slow down the progression of myopia. The side effects include dilation of the pupil, sensitivity to light, and loss of focusing.”
In my experience, these problems are minimal with the use progressives to eliminate the effects of paresis of accommodation, and Transitions to reduce the sensitivity to light. Of more than 40 patients who used atropine, I have had only one patient stop the treatment due to light sensitivity. Another developed an allergy, but didn’t want to stop treatment, so we added one drop of Lotemax 20 minutes prior to the instillation of atropine.
The decision to be placed on atropine is not my decision; it is the patient/parent with full discussion of the risk and benefits. The patient returns three months after atropine treatment begins. I am always amazed at the lack of complaints. Pupillary dilation is much less than with tropicamide and even less than cyclopentolate; kids learn to use progressives immediately.
Take for example a family in which all the older siblings, like the parents, are myopic in the range -10.00D to -14.00D. You are now examining their 6-year-old child who demonstrates -2.50 O.U. on his first examination. Do you consider it appropriate with all the myopia studies not to offer atropine treatment? In my experience, these parents, after listening to the risks and benefits, elect to begin treatment with atropine. In my experience, the myopic progression slows to less than 0.50D per year—extremely impressive.
Or take the five-year-old child who presented to me bumping into walls, showing slow development, and refracted to -12.00 upon first examination. Would it be proper or fair with the abundant literature not to offer this child atropine treatment? We did and I am happy to report five years later that his refractive error has remained stable. As a side note: atropine has been shown to stabilize myopia in the higher refractive errors.
I agree that atropine treatment is not currently the standard of care, but maybe it should be. I completely disagree with your biased statement, “atropine therapy is not appropriate for most children.” In my opinion, it should be offered to any myopic patient interested in stropping the progression of myopia. The risks are low; the medication has been prescribed in patients for years to control uveitis without any evidence of long-term side effects. I believe it is the role of the doctor to make the correct diagnosis, and then present current treatment options explaining risks and benefits to the patient. Many of our patients, after listening to their options, elect single vision lenses, others progressive lenses, others atropine, and lastly others multifocal contact lenses. Once children have reached that contact lens age, our current treatment of choice is a multifocal contact lens, though there is a paucity of information about its efficacy.
Lastly, though we do not know the exact mechanism of atropine in slowing down myopia, we know that it is not accommodation or cycloplegia. There have been a number of ingenious animal studies investigating the efficacy of atropine.26-28 For example, cutting the optic nerve of a chick, thus eliminating the feedback mechanism of accommodation and blur, does not diminish the effect of atropine; and segmental diffusers, which are not accommodation based, result in segmental or regional elongation of the eyeball. These observations led to the development of pirenzepine, which unlike atropine (a non-specific anti-cholinergic muscarinic drug), is a specific anti-muscarinic medication and does not effect accommodation.29-31 It seems that atropine and other muscarinic drugs somehow block a bio-chemical signal originating in the ciliary body signaling the eye to elongate.
Remember what the 19th-century philosopher Arthur Schopenhauer said: “All truth passes through three stages. First, it is ridiculed. Second, it is violently opposed. And third, it is accepted as being self-evident.” Treatment of myopia with atropine is in the second stage. Either it will pass to the third stage or a better “atropine” will come in to use. Right now atropine is the only effective method to retard the progression of myopia and should be in optometry’s armament to fight the effects of myopia.
—Jeffrey Cooper M.S., O.D., Clinical Professor of Optometry
SUNY State College of Optometry
Drs. Chou and Legerton respond:
We’d like to thank Dr. Cooper for his interest in myopia regulation. As mentioned in our article, the efficacy of atropine for minimizing myopia progression is well established. Still, few practitioners prescribe atropine for myopic children.
According to Dr. Cooper, this is because atropine lacks approval for myopia regulation and is generically available. We respectfully disagree. Consider that no excimer laser manufacturer had approval for LASIK until 1999. Yet prior to that date, LASIK was routinely performed off-label. Avastin (bevacizumab, Genentech), despite its lack of approval for AMD, is routinely used by retinal specialists for that purpose. The LASIK and Avastin examples demonstrate how FDA approval and the consequent capacity for manufacturer promotion are not required for widespread adoption of a medical instrument or drug.
Though clinicians have known of atropine’s efficacy for myopia control for more than three decades, why isn’t atropine used more? We believe undesirable attributes of atropine sabotage its demonstrated efficacy against myopic progression. In particular, the mydriasis and cycloplegia with atropine are undeniable. Yet there is a scarcity of evidence to assure a parent that their child’s unusually large pupils and accommodative paresis will not lead to light sensitivity, peer ostracization and bullying, and reduced visual performance for academics and athletics. Clinicians have an ethical responsibility to ensure that attempts to mitigate myopia do not compromise a child’s social, educational, and physical development. This is particularly important because children don’t always complain.
Dr. Cooper has expressed his opinion that atropine for controlling childhood myopia should become the standard of care. From our individual experiences providing medical-legal expert testimony, we believe that legal terms deserve precise use. “Standard of care” is defined as the level at which the average, prudent provider in a given community would practice. Breach of standard of care constitutes negligence. Hence, if Dr. Cooper believes atropine treatment is the standard of care, by extension, any practitioner not prescribing atropine for childhood myopia is negligent.
Our opinion is that practitioners are well justified, if not compassionate, to omit atropine treatment for myopia regulation.
1. Gwiazda JE, Hyman L, Norton TT, Hussein ME, Marsh-Tootle W, Manny R, et al. Accommodation and related risk factors associated with myopia progression and their interaction with treatment in COMET children. Invest Ophthalmol Vis Sci 2004;45(7):2143-51.
2. Gwiazda J. Treatment options for myopia. Optom Vis Sci 2009;86(6):624-8.
3. Young FA. The Effect of Atropine on the Development of Myopia in Monkeys. Am J Optom Arch Am Acad Optom 1965;42:439-49.
4. Bedrossian RH. The effect of atropine on myopia. Ann Ophthalmol 1971;3(8):891-7.
5. Gimbel HV. The control of myopia with atropine. Can J Ophthalmol 1973;8(4):527-32.
6. Bedrossian RH. The effect of atropine on myopia. Ophthalmology 1979;86(5):713-9.
7. Dyer JA. Role of cyclopegics in progressive myopia. Ophthalmology 1979;86(5):692-4.
8. Brodstein RS, Brodstein DE, Olson RJ, Hunt SC, Williams RR. The treatment of myopia with atropine and bifocals. A long-term prospective study. Ophthalmology 1984;91(11):1373-9.
9. Bedrossian RH. The treatment of myopia with atropine and bifocals: a long-term prospective study. Ophthalmology 1985;92(5):716.
10. Brenner RL. Further observations on use of atropine in the treatment of myopia. Ann Ophthalmol 1985;17(2):137-40.
11. Gruber E. Treatment of myopia with atropine and bifocals. Ophthalmology 1985;92(7):985.
12. Yen MY, Liu JH, Kao SC, Shiao CH. Comparison of the effect of atropine and cyclopentolate on myopia. Ann Ophthalmol 1989;21(5):180-2, 87.
13. Chou AC, Shih YF, Ho TC, Lin LL. The effectiveness of 0.5% atropine in controlling high myopia in children. J Ocul Pharmacol Ther 1997;13(1):61-7.
14. Kennedy RH, Dyer JA, Kennedy MA, Parulkar S, Kurland LT, Herman DC, et al. Reducing the progression of myopia with atropine: a long term cohort study of Olmsted County students. Binocul Vis Strabismus Q 2000;15(3 Suppl):281-304.
15. Palmer EA. More on the medical management of school myopia. Binocul Vis Strabismus Q 2000;15(4):319-20.
16. Pointer RW. Atropine and photochromic bifocals for 800 cases of school myopia. Binocul Vis Strabismus Q 2000;15(3):256.
17. Romano PE, Donovan JP. Management of progressive school myopia with topical atropine eyedrops and photochromic bifocal spectacles. Binocul Vis Strabismus Q 2000;15(3):257-60.
18. Chiang MF, Kouzis A, Pointer RW, Repka MX. Treatment of childhood myopia with atropine eyedrops and bifocal spectacles. Binocul Vis Strabismus Q 2001;16(3):209-15.
19. Romano PE. There's no longer any need for randomized control groups; it's time to regularly offer atropine and bifocals for school myopia; comments on evidence-based medicine. Binocul Vis Strabismus Q 2001;16(1):12.
20. Shih YF, Hsiao CK, Chen CJ, Chang CW, Hung PT, Lin LL. An intervention trial on efficacy of atropine and multi-focal glasses in controlling myopic progression. Acta Ophthalmol Scand 2001;79(3):233-6.
21. Syniuta LA, Isenberg SJ. Atropine and bifocals can slow the progression of myopia in children. Binocul Vis Strabismus Q 2001;16(3):203-8.
22. Chua WH, Balakrishnan V, Chan YH, Tong L, Ling Y, Quah BL, et al. Atropine for the treatment of childhood myopia. Ophthalmology 2006;113(12):2285-91.
23. Lee JJ, Fang PC, Yang IH, Chen CH, Lin PW, Lin SA, et al. Prevention of myopia progression with 0.05% atropine solution. J Ocul Pharmacol Ther 2006;22(1):41-6.
24. Fan DS, Lam DS, Chan CK, Fan AH, Cheung EY, Rao SK. Topical atropine in retarding myopic progression and axial length growth in children with moderate to severe myopia: a pilot study. Jpn J Ophthalmol 2007;51(1):27-33.
25. Tong L, Huang XL, Koh AL, Zhang X, Tan DT, Chua WH. Atropine for the treatment of childhood myopia: effect on myopia progression after cessation of atropine. Ophthalmology 2009;116(3):572-9.
26. McBrien NA, Moghaddam HO, Reeder AP. Atropine reduces experimental myopia and eye enlargement via a nonaccommodative mechanism. Invest Ophthalmol Vis Sci 1993;34(1):205-15.
27. Schaeffel F, Troilo D, Wallman J, Howland HC. Developing eyes that lack accommodation grow to compensate for imposed defocus. Vis Neurosci 1990;4(2):177-83.
28. Troilo D, Gottlieb MD, Wallman J. Visual deprivation causes myopia in chicks with optic nerve section. Curr Eye Res 1987;6(8):993-9.
29. Truong HT, Cottriall CL, Gentle A, McBrien NA. Pirenzepine affects scleral metabolic changes in myopia through a non-toxic mechanism. Exp Eye Res 2002;74(1):103-11.
30. Leech EM, Cottriall CL, McBrien NA. Pirenzepine prevents form deprivation myopia in a dose dependent manner. Ophthalmic Physiol Opt 1995;15(5):351-6.
31. Le QH, Cheng NN, Wu W, Chu RY. Effect of pirenzepine ophthalmic solution on form-deprivation myopia in the guinea pigs. Chin Med J (Engl) 2005;118(7):561-6.