Methods of Myopia Control; the Scientific Studies and What They Say
Grovesnor T. in “Myopia: what can we do about it clinically?”1 discusses Methods that have been used by vision practitioners for the control of myopia including visual training, biofeedback training, undercorrection, overcorrection, the use of bifocal lenses, the use of contact lenses, the instillation of atropine, and refractive surgery. He notes that with some exceptions the use of these methods has achieved only limited success. The lack of success with the less-invasive methods–which are based on the supposition that myopia is caused by accommodation–may be due to the fact that they are used for eyes that are already myopic and therefore have already undergone axial elongation and scleral stretching. If it were possible to predict which children were at risk for the development of myopia, vision practitioners would be able to institute procedures for the control of myopia when only a minimum of scleral stretching has occurred. Risk factors that warrant investigation include the axial length/corneal radius ratio and the resting state of accommodation.
Young FA. in “The nature and control of myopia”2 notes there is a growing body of evidence to support the belief that most myopia develops as a result of prolonged exposure to nearpoint activities. This paper summarizes the most important studies that have been done and postulates a mechanism by which prolonged accommodation can result in myopia. Possible means of arresting or preventing the development of myopia are discussed.
Wallman J, et al. In “Local retinal regions control local eye growth and myopia.3 note “In chicks, visual deprivation leads to myopia and enlargement of the vitreous chamber of the eye. When chicks were raised with white translucent occluders over their eyes so that either the nasal half, the temporal half, or all of the retina was visually deprived, the resulting myopia (median = -15 diopters) was limited to the deprived part of the retina, regardless of which half of the retina was visually deprived; the nondeprived part remained nearly emmetropic. Correspondingly, the vitreous chamber was elongated only in the region of the visual deprivation, resulting in eyes with different asymmetric shapes depending on which retinal region was deprived. These results argue for a local regulation of ocular growth that is dependent on vision and suggest a hypothesis to explain the epidemiological association of myopia in humans with large amounts of reading. Because most nonfoveal retinal neurons have large receptive fields, they cannot resolve the individual letters on the printed page; this may lead to their activity being less during reading than during most other forms of visual stimulation. Thus, the impoverished stimulus situation of reading may lead to myopia, as do other types of visual form deprivation.”
Zadnik K, Mutti DO. In “How applicable are animal myopia models to human juvenile onset myopia?4 and Christensen AM et al. in “Evidence that increased scleral growth underlies visual deprivation myopia in chicks”5 evaluated three measures of scleral growth in chicks that were visually deprived with the use of translucent occluders. The authors sought to determine whether the ocular elongation and myopia that results from this deprivation is associated with increased growth of the sclera. The authors found that the dry weight of the sclera of deprived eyes increased 65% faster than that of nondeprived eyes. Furthermore, the uptake of labeled methionine and thymidine was significantly increased by visual deprivation, whether expressed as incorporation per sclera, per milligram of sclera, per milligram of protein, or per milligram of DNA. In addition, the amount of DNA and soluble protein was significantly greater in the scleras of deprived eyes than in those of nondeprived eyes. Finally, the degree of hydration of the scleras from deprived eyes was greater relative to their weight than that of the scleras from nondeprived eyes. These results suggest that visual deprivation causes increased cellular proliferation and increased protein synthesis in the sclera of chicks.
In the study “Myopia: attempts to arrest progression.”6 the authors note “previous studies have evaluated the efficacy of several interventions to decrease the progression of myopia. These include devices that alter the perception of the visual environment and pharmacological treatments. There is no conclusive evidence thus far that alteration of the pattern of spectacle wear, bifocals, ocular hypotensives, or contact lenses retards the progression of myopia. Several randomised clinical trials have demonstrated that the rate of progression of myopia is lower in children given atropine eye drops than those given placebo. However, atropine is associated with short term side effects such as photophobia and possible long term adverse events including light induced retinal damage and cataract formation. Other more selective antimuscarinic agents such as pirenzipine are presently being evaluated. Further well conducted randomised clinical trials with large sample sizes and adequate follow up designed to evaluate treatments to retard the progression of myopia should be conducted, since the identification of an effective intervention may have a greater public health impact on the burden and morbidity from myopia than the few treatments currently available.”
1Optom Vis Sci. 1989 Jul;66(7):415-9
2J Am Optom Assoc. 1977 Apr;48(4):451-7
3Science. 1987 Jul 3;237(4810):73-7
4Vision Res. 1995 May;35(9):1283-8
5Invest Ophthalmol Vis Sci. 1991 Jun;32(7):2143-50
6Br J Ophthalmol. 2002 Nov;86(11):1306-11