Article Date: 6/1/2011

Correcting Lenses Can Alter Refractive Development
TOPIC: Contact Lenses and Myopia Control: Evidence Versus Hype

Point

Correcting Lenses Can Alter Refractive Development

By Earl L. Smith III, OD, PhD, FAAO

The broader issue is whether correcting lenses in general can alter refractive development and, specifically, reduce myopia progression.

Myopic Defocus is Promising

A large body of research on a wide range of laboratory animals has demonstrated conclusively that refractive development is regulated by the eye's effective refractive state and that correcting lenses, by changing the eye's effective refraction, can predictably alter eye growth and the course of refractive development (Smith III and Hung, 1999; Wallman and Winawer, 2004). These studies have demonstrated that myopic defocus imposed across a large proportion of the visual field can slow axial elongation and produce relative hyperopic shifts in refraction.

But the key issue is whether clinically significant reductions in myopia progression are possible with traditional lenses. On this issue, the evidence to date is weaker, but it is getting stronger rapidly. For instance, in a recent, large-scale study that employed executive bifocals, which effectively produced myopic defocus over a much larger portion of the visual field compared to progressive addition lenses, myopia progression was reduced almost by half (Cheng et al, 2010), which I believe is clinically meaningful.

Evidence With Contact Lenses

The results associated with a number of different contact lens designs are very promising. Early small-scale studies indicated that overnight orthokeratology was clinically effective in reducing myopia progression (Cho et al, 2005; Walline et al, 2009). These positive findings have recently been replicated in a larger prospective study published out of Japan (Kakita et al, 2011) and are further supported by the interim results from three ongoing prospective trials (Cheung and Cho 2010; Santodomingo-Rubido et al, 2010; Swarbrick, et al, 2011). Results from laboratory animals suggest that the positive treatment effects from orthokeratology come about because the induced changes in corneal power produce relative myopia over a large part of the peripheral visual field (Smith III et al, 2005; Charman et al, 2006; Liu and Wildsoet, 2010). In this respect, newly developed contact lenses that specifically target the pattern of peripheral refractions and that selectively reduce the degree of relative peripheral hyperopia can decrease myopia progression in children by 36 percent over a 12-month trial (Holden et al, 2010).

Promising results have also been obtained using multifocal contact lenses that have optical profiles similar to concentric bifocals and that produce relative myopic defocus in both the peripheral and central fields simultaneously (Aller and Wildsoet, 2008; Lam et al, 2010; Anstice and Phillips, 2011). The resulting reductions in myopia progression with these contact lens strategies are clinically significant. Moreover, it is likely that the effectiveness of these contact lens designs can be improved. It will be important to improve the efficacy of these lenses, because optical treatment strategies will not eliminate existing myopic errors. Instead, they will probably only slow subsequent progression.

The Evidence is Strong

The encouraging results described above have yet to be confirmed in gold-standard clinical trials (some are currently ongoing). Nonetheless, I think that the evidence supports the hype and that it is very reasonable to present these options to patients while clearly communicating the preliminary nature of the results associated with these promising new designs. CLS

For references, please visit www.clspectrum.com/references.asp and click on document #187.


Professor Smith currently holds the Greeman-Petty Professorship in Vision Development and is serving as the dean of the College of Optometry at the University of Houston. His research interests are focused on the optics of the eye. He received the Glenn Fry Award (1996) and the Prentice Medal (2010) from the American Academy of Optometry for his research on the role of vision in regulating refractive development and eye growth. He has proprietary interest in products manufactured by Ciba Vision and Zeiss Optical.

Counterpoint

Peripheral Myopic Defocus May Not be the Answer

By Donald O. Mutti, OD, PhD

The history of treatments to slow myopia progression is one of early promise not borne out by later work. Conventionally fitted rigid contact lenses were supposed to halt progression. Later rigorous clinical trials showed that they had no real effect on axial growth (Katz et al, 2003; Walline et al, 2004). Bifocal spectacles were also touted, but did not produce significant results (Grosvenor et al, 1987).

The bifocal emphasis then shifted to children who had near-point esophoria. Rigorous clinical evaluation showed that bifocals in esophores had an effect, but only a modest 0.25D slower progression in 2.5 years (Fulk et al, 2000). Progressive addition lens (PAL) designs were then supposed to be the better bifocal. When fully studied, these also produced only a modest effect, 0.20D of benefit over three years (Gwiazda et al, 2003). PALs were then proposed to work better in esophores who had a high accommodative lag. Once again, a prospective randomized clinical trial showed that the benefit was a modest 0.28D over three years (COMET 2, 2011).

Atropine, the biggest anti-myopia gun we have, might not even work that well. Treatment benefit may saturate after the first year or so with parallel progression rates in later years for treated and control eyes (Gimbel, 1973). The benefit of atropine treatment, a respectable 0.92D in two years, largely disappeared from rebound by 0.76D after one year off treatment (Tong et al, 2009).

Studying Defocus Strategies

Proper treatment should begin with the proper theory about myopia etiology. Most in the field would argue that hyperopic retinal defocus drives myopic eye growth. This argument is based on nearly 25 years of data from animal experimentation showing a reliable vitreous elongation in response to minus lenses placed over the eyes of young animals. Despite the wealth of animal evidence, this hypothesis simply has not translated into useful predictions about human development (Mutti et al, 2009; Mutti et al, 2006; Berntsen et al, in press).

So now we turn from the fovea to the periphery. The animal data supporting this revised hypothesis are excellent. Nevertheless, the hypothesis still rests on the belief that defocus is a visual signal for ocular growth. And once again, the human data suggest that peripheral defocus is no better than foveal defocus as a growth signal for human myopia onset or progression (Mutti et al, 2011).

Seeking the Burden of Proof

Treatments supplying peripheral myopia might work, and I hope that they do. As in all of myopia control history, the proof is in the randomized clinical trial. So far we have not had the randomized, long-term (three years at a minimum) clinical trial of a myopia treatment aimed at altering peripheral defocus. The data we do have are very provocative, but preliminary. A recent specialty spectacle study still only had an effect size of 0.29D (Sankaridurg et al, 2010). Overnight orthokeratology shows more promise (Walline et al, 2009).

We are fortunate to have the technology to perform complete biometry, to reliably measure ocular shape, axial length, and now even choroidal thickness. As these clinical trials are conducted, let's make sure that the 0.25D or so that has been the treatment effect size over and over again is not 100 microns or so of choroidal thickening from myopic defocus. What we really want is effective slowing of ocular growth. In the meantime, we need to guard against expectations taking over the debate before we see results from the definitive clinical trials to come. CLS

For references, please visit www.clspectrum.com/references.asp and click on document #187.


Dr. Mutti is currently the E.F. Wildermuth Foundation Professor in Optometry at The Ohio State University College of Optometry. He is a co-investigator with Dr. Karla Zadnik on the Collaborative Longitudinal Evaluation of Ethnicity and Refractive Error (CLEERE) study, a National Eye Institute funded study of refractive error and normal eye growth now in its twentieth year. He is also a consultant or advisor to Vistakon and has received lecture or authorship honoraria from B+L.

Contact Lens Spectrum, Issue: June 2011