- Email: [email protected]
Are we myopic about myopia control?
G Model CLAE-703; No. of Pages 3
ARTICLE IN PRESS Contact Lens & Anterior Eye xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
Contact Lens & Anterior Eye journal homepage: www.elsevier.com/locate/clae
Editorial
Are we myopic about myopia control?
The ability to slow down or stop the progression of myopia through pharmacological and optical means is well accepted in the scientific literature. More recently the topic of myopia control is gaining momentum at clinical conferences, with the practitioner now permitted a selection of evidence based modalities to employ in this pursuit, the most promising of which are in the contact lens arena. Yet speaking to my clinical colleagues still yields a sense of hesitation to fully embrace myopia management. I hear concerns that the risk of paediatric contact lens wear must surely outweigh the increased risk of ocular pathology brought about by higher myopia. I am asked – what’s the difference between −2.00 and −3.00 anyway? More evidence is needed, I am told. Speaking to academic colleagues reveals a sense of frustration that knowledge gains do not appear to be treated with clinical eagerness – that perhaps they are diluted in translation. There appears to be a delay in years between the theory and the practice of myopia control. This is evidenced in static contact lens wear age demographics and declines in rigid lens fitting over time [1] – although small increases are recorded in orthokeratology fits, they still account for only 1% of all contact lens fits across the world [2]. Academic leaders and clinical trailblazers continuously steer the profession towards better patient outcomes. In the contact lens sphere, historical clinical challenges have been solved by science and translated into practice, such as hypoxia, or complications from older lens designs and care systems. Some puzzles remain unsolved, such as predictability of multifocal contact lens success, and reducing infective and inflammatory events. Myopia control sits across multiple areas of research expertise, from optics to epidemiology to animal studies. Synthesis of this information into clinical form may be an equal challenge to finding the scientific answers. Being involved in anterior eye research and also in contact lens clinical practice puts me in an interesting position to attempt this synthesis through recent conference presentations on the topic. Encompassing literature review related to my research, personal learning has led to increased fervour to help translate science to clinical management pathways beyond the walls of my practice. Myopia control is of high importance to the entire eye care sector, and is not just the realm of the paediatric practitioner or the contact lens specialist. As practitioners we demonstrate our own myopia when espousing that the immediate risks of myopia control modalities outweigh future risks of ocular complications.
1. Taking myopia seriously Perhaps myopia is regarded more as an inconvenience than a disease, especially in lower levels. However myopia management must be taken seriously because of the potential to modify a patient’s lifetime risk of sight threatening sequelae such as myopic maculopathy, cataract, glaucoma and retinal detachment. An earlier age of onset is linked to faster myopic progression, which in turn contributes to increased severity and higher risk of these ocular complications [3–5]. It is commonly held that there is a difference between physiological and pathological myopia, which is arbitrarily defined as 5–6D. However Flitcroft [6] makes the convincing argument that even at 1D of myopia, there is additional pathological risk carried over the emmetrope. Being a low myope of one to three dioptres doubles the odds of myopic maculopathy, triples to quadruples the odds of retinal detachment, and doubles risk of glaucoma and posterior subcapsular cataract [4,6–8] .I’ve been rather pleased with my 1D of myopia over the past 15 years and know I’ll be even more pleased with it in my 40’s, but am wrong to consider it benign. Atrophic myopic maculopathy is a significant cause of blindness in the working population and little advancement has been made in its treatment compared to other ocular pathologies like glaucoma and cataract [6]. Flitcroft’s calculations showed a 60 fold increase in prevalence of myopic maculopathy over 5D compared to lower myopes; even at 3D of myopia, though, there is an almost 10 fold increase in risk. These are startling facts. However it is understandable that the practitioner may not see the lifetime clinical picture of the myope with the risks of paediatric contact lens wear looming in the foreground. Well accepted is the propensity for orthokeratology [9–15] and multifocal soft contact lenses [16–18] to slow progression of myopia. Certainly, the risk of microbial keratitis in contact lens wear is immediate whereas the future risk of glaucoma, or retinal detachment following cataract surgery, does not sit top of mind with a paediatric patient. The evidence, though, demands a long-sighted focus in paediatric myopia management. The incidence of ulcerative keratitis in the non contact lens wearing population is 0.014%, and 0.131% in the contact lens wearing population [19]. By comparison, glaucoma incidence is 4.2% in low myopia (1–3D) and 4.4% in eyes over 3D [4]. Retinal detachment after cataract surgery has an incidence of 1.69% in high myopia [20], and 4.6% after prior repair or retinal breaks or detachment [21], which is more likely in the myope. Comparison
http://dx.doi.org/10.1016/j.clae.2014.05.004 1367-0484/© 2014 British Contact Lens Association. Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Johnson KL. Are we myopic about myopia control? Contact Lens Anterior Eye (2014), http://dx.doi.org/10.1016/j.clae.2014.05.004
G Model CLAE-703; No. of Pages 3
ARTICLE IN PRESS Editorial / Contact Lens & Anterior Eye xxx (2014) xxx–xxx
2
of these percentages paints a convincing picture for our paediatric low myope considering contact lens wear – he or she is 32 times more likely to suffer glaucoma than microbial keratitis. If we can keep a 1D myope out of the next effective risk bracket of 3D, this will mean a reduction in risk odds by 4–5 times for myopic maculopathy, three times for retinal detachment and one and a half times for posterior subcapsular cataract [6]. If this myope instead reaches 5D, they are still 12 times more likely to suffer retinal detachment than contact lens related microbial keratitis. The latter debunks the ‘why bother’ argument of myopia control. The ‘who’ is still unanswered – I understand my clinical colleagues’ hesitation in applying scientific myopia control results to clinical practice. Application of research outcomes to different age and ethnic groups in clinical practice is problematic. Some percentage of children still progress significantly, despite intervention [22]. Most myopia control studies are of one to two years duration, and longer studies have generally shown diminishing results. Percentage rates of myopia control can be difficult to understand. While methodologically sound, an impressive percentage can sometimes translate to 0.25D/year less progression which is clinically unimpressive. We are also yet to find the answer to preventing myopia – an at-risk child must wait for time to take its course and myopia to take hold before we can apply myopia control therapy. We have some understanding of pre-myopia risks, such as family history, binocular vision function, environmental influence and peripheral optics, but all suffer conjecture. Brennan levelled the playing field through evidence that reducing the progression of myopia by 33% would result in a 73% reduction in the frequency of myopia over 5D, and if progression was reduced by 50% this would mean 90% less high myopia [23]. While ‘pathological’ myopia is earnestly regarded, Flitcroft argues that there may be no ‘physiological’ level of myopia where safety of ocular health is outweighed by the minimal benefits of low myopia [6]. Has the time arrived to consider fitting contact lenses for myopia control as a medical necessity, as for keratoconus or aphakia? What further evidence do we need? 2. The clinical myopia profile In the past I found myself having lengthy conversations with parents of myopic children about risk factors for progression, and mechanisms of myopia control. Covering a vast array of literature verbally often resulted in blank stares and a late appointment schedule. In response I developed a Clinical Myopia Profile, which is a communication tool collating a paediatric patient’s risk factors for both myopia development and progression in view of the scientific literature. While best constructed from the individual practitioner’s own understanding and methods of explanation, colleagues around the world have responded favourably to my attempt at synthesising the scientific literature into clinical information, and I have been happy to share it. A child’s binocular vision status, age and refraction, family history, visual tasks, home and leisure environment, and capabilities with modality options must all be considered in profiling myopia. Any parental history of myopia should be an initial trigger to evaluate binocular vision risk factors in the emmetropic child and determine any state of pre-myopia, including lesser levels of paediatric age-normal hyperopia [24]. While there is conjecture [25], managing esophoria and accommodative lag [26–28], and providing advice on environmental risk factors [29], is the limit of evidence-based myopia management for at-risk emmetropes at this point in time. Because of the evidence that there may be no ‘safe’ level of myopia which could be considered physiological, it may not demonstrate best practice clinical care to wait until a child demonstrates consistent progression before commencing myopia control
contact lens wear. Lower levels of myopia which may not traditionally indicate a lifestyle need for contact lens wear, such as the 1D myope without sport participation concerns, should also be considered for active myopia management. Clinical conundrums still exist for the stable paediatric myope; the astigmatic myope where both multifocal and OK visual outcomes may be compromised; the child with severe binocular vision issues who does not achieve control with contact lenses alone; partial correction for higher myopes [30]; children who are contraindicated for contact lens wear; and patients with anatomical limitations for contact lens wear such as East Asian eyelid anatomy affecting OK lens centration. Myopia control is important beyond the lifestyle benefits of contact lens wear and the feelgood factor of a lower prescription – reduction of future ocular health risk is paramount. These risks of myopic maculopathy, glaucoma, retinal detachment and cataract are frequently greater than the risk of serious contact lens complications, and it is crucial to spread the word on this account. Determination of clinical management pathways for myopia are desired, and should remain a hot topic over the coming years, as mechanisms of myopia control are further revealed and novel methods emerge. A combined approach will be required to tackle the unanswered scientific questions and the clinical conundrums, and to then ensure education of young myopes and their parents towards better patient outcomes. References [1] Morgan PB, Efron N. A decade of contact lens prescribing trends in the United Kingdom (1996–2005). Cont Lens Anterior Eye 2006;29:59–68. [2] Efron N, Morgan PB, Woods CA. International survey of rigid contact lens fitting. Optom Vis Sci 2013;90:113–8. [3] Saw S-M, Gazzard G, Shih-Yen EC, Chua W-H. Myopia and associated pathological complications. Ophthal Physiol Opt 2005;25:381–91. [4] Mitchell P, Hourihan F, Sandbach J, Wang JJ. The relationship between glaucoma and myopia: the Blue Mountains Eye Study. Ophthalmology 1999;106:2010–5. [5] Lin LL-K, Shih Y-F, Tsai C-B, Chen C-Y, Lee L-A, Hung P-T, et al. Epidemiologic study of ocular refraction among schoolchildren in Taiwan in 1995. Optom Vis Sci 1999;76:275–81. [6] Flitcroft DI. The complex interactions of retinal, optical and environmental factors in myopia aetiology. Prog Retin Eye Res 2012;31:622–60. [7] Vongphanit J, Mitchell P, Wang JJ. Prevalence and progression of myopic retinopathy in an older population. Ophthalmology 2002;109:704–11. [8] Li X. Incidence and epidemiological characteristics of rhegmatogenous retinal detachment in Beijing, China. Ophthalmology 2003;110:2413–7. [9] Cho P, Cheung SW, Edwards M. The Longitudinal Orthokeratology Research in Children (LORIC) in Hong Kong: a pilot study on refractive changes and myopic control. Curr Eye Res 2005;30:71–80. [10] Walline JJ, Jones LA, Sinnott LT. Corneal reshaping and myopia progression. Br J Ophthalmol 2009;93:1181–5. [11] Swarbrick HA, Alharbi A, Watt K, Lum E. Overnight orthokeratology lens wear slows axial eye growth in myopic children. Invest Ophthalmol Vis Sci 2010;51:1721. [12] Kakita T, Hiraoka T, Oshika T. Influence of overnight orthokeratology on axial elongation in childhood myopia. Invest Ophthalmol Vis Sci 2011;52:2170–4. [13] Cho P, Cheung S-W. Orthokeratology for slowing myopic progression: a randomised controlled trial. Cont Lens Anterior Eye 2011;34:S2–3. [14] Hiraoka T, Kakita T, Okamoto F, Takahashi H, Oshika T. Long-term effect of overnight orthokeratology on axial length elongation in childhood myopia: a 5-year follow-up study. Invest Ophthalmol Vis Sci 2012;53:3913–9. [15] Charm J, Cho P. High myopia-partial reduction ortho-k: a 2-year randomized study. Optom Vis Sci 2013;90:530–9. [16] Anstice NS, Phillips JR. Effect of dual-focus soft contact lens wear on axial myopia progression in children. Ophthalmology 2011;118:1152–61. [17] Sankaridurg P, Holden B, Smith 3rd E, Naduvilath T, Chen X, de la Jara P, et al. Decrease in rate of myopia progression with a contact lens designed to reduce relative peripheral hyperopia: one-year results. Invest Ophthalmol Vis Sci 2011;52:9362–7. [18] Walline JJ, Greiner KL, McVey ME, Jones-Jordan LA. Multifocal contact lens myopia control. Optom Vis Sci 2013;90:1207–14. [19] Jeng BH, Gritz DC, Kumar AB, Holsclaw DS, Porco TC, Smith SD, et al. Epidemiology of ulcerative keratitis in Northern California. Arch Ophthalmol 2010;128:1022–8. [20] Fan DS, Lam DS, Li KK. Retinal complications after cataract extraction in patients with high myopia. Ophthalmology 1999;106:688–91 [discussion 91–2]. [21] Grand MG. The risk of a new retinal break or detachment following cataract surgery in eyes that had undergone repair of phakic break or detachment: a hypothesis of a causal relationship to cataract surgery. Trans Am Ophthalmol Soc 2003;101:335–69.
Please cite this article in press as: Johnson KL. Are we myopic about myopia control? Contact Lens Anterior Eye (2014), http://dx.doi.org/10.1016/j.clae.2014.05.004
G Model CLAE-703; No. of Pages 3
ARTICLE IN PRESS Editorial / Contact Lens & Anterior Eye xxx (2014) xxx–xxx
[22] Chan KY, Cheung SW, Cho P. Orthokeratology for slowing myopic progression in a pair of identical twins. Cont Lens Anterior Eye 2014;37: 116–9. [23] Brennan NA. Predicted reduction in high myopia for various degrees of myopia control. Cont Lens Anterior Eye 2012;35S1:e14–5. [24] Mutti DO, Hayes JR, Mitchell GL, Jones LA, Moeschberger ML, Cotter SA, et al. Refractive error, axial length, and relative peripheral refractive error before and after the onset of myopia. Invest Ophthalmol Vis Sci 2007;48:2510–9. [25] Mutti DO, Mitchell GL, Hayes JR, Jones LA, Moeschberger ML, Cotter SA, et al. Accommodative lag before and after the onset of myopia. Invest Ophthalmol Vis Sci 2006;47:837–46. [26] Nakatsuka C, Hasebe S, Nonaka F, Ohtsuki H. Accommodative lag under habitual seeing conditions: comparison between myopic and emmetropic children. Jpn J Ophthalmol 2005;49:189–94. [27] Gwiazda J, Grice K, Thorn F. Response AC/A ratios are elevated in myopic children. Ophthalmic Physiol Opt 1999;19:173–9.
3
[28] Gwiazda J, Thorn F, Held R. Accommodation, accommodative convergence, and response AC/A ratios before and at the onset of myopia in children. Optom Vis Sci 2005;82:273–8. [29] Rose KA, Morgan IG, Ip J, Kifley A, Huynh S, Smith W, et al. Outdoor activity reduces the prevalence of myopia in children. Ophthalmology 2008;115:1279–85. [30] Charm J, Cho P. High myopia-partial reduction orthokeratology (HM-PRO): study design. Cont Lens Anterior Eye 2013;36:164–70.
Kate L. Johnson (BAppSc(Optom)Hons, GCOT, FBCLA, FIACLE, FCCLSA, FAAO) Gerry & Johnson Optometrists, Level 4, 217 George Street, Brisbane, QLD 4000, Australia E-mail address: [email protected]
Please cite this article in press as: Johnson KL. Are we myopic about myopia control? Contact Lens Anterior Eye (2014), http://dx.doi.org/10.1016/j.clae.2014.05.004
ARTICLE IN PRESS Contact Lens & Anterior Eye xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
Contact Lens & Anterior Eye journal homepage: www.elsevier.com/locate/clae
Editorial
Are we myopic about myopia control?
The ability to slow down or stop the progression of myopia through pharmacological and optical means is well accepted in the scientific literature. More recently the topic of myopia control is gaining momentum at clinical conferences, with the practitioner now permitted a selection of evidence based modalities to employ in this pursuit, the most promising of which are in the contact lens arena. Yet speaking to my clinical colleagues still yields a sense of hesitation to fully embrace myopia management. I hear concerns that the risk of paediatric contact lens wear must surely outweigh the increased risk of ocular pathology brought about by higher myopia. I am asked – what’s the difference between −2.00 and −3.00 anyway? More evidence is needed, I am told. Speaking to academic colleagues reveals a sense of frustration that knowledge gains do not appear to be treated with clinical eagerness – that perhaps they are diluted in translation. There appears to be a delay in years between the theory and the practice of myopia control. This is evidenced in static contact lens wear age demographics and declines in rigid lens fitting over time [1] – although small increases are recorded in orthokeratology fits, they still account for only 1% of all contact lens fits across the world [2]. Academic leaders and clinical trailblazers continuously steer the profession towards better patient outcomes. In the contact lens sphere, historical clinical challenges have been solved by science and translated into practice, such as hypoxia, or complications from older lens designs and care systems. Some puzzles remain unsolved, such as predictability of multifocal contact lens success, and reducing infective and inflammatory events. Myopia control sits across multiple areas of research expertise, from optics to epidemiology to animal studies. Synthesis of this information into clinical form may be an equal challenge to finding the scientific answers. Being involved in anterior eye research and also in contact lens clinical practice puts me in an interesting position to attempt this synthesis through recent conference presentations on the topic. Encompassing literature review related to my research, personal learning has led to increased fervour to help translate science to clinical management pathways beyond the walls of my practice. Myopia control is of high importance to the entire eye care sector, and is not just the realm of the paediatric practitioner or the contact lens specialist. As practitioners we demonstrate our own myopia when espousing that the immediate risks of myopia control modalities outweigh future risks of ocular complications.
1. Taking myopia seriously Perhaps myopia is regarded more as an inconvenience than a disease, especially in lower levels. However myopia management must be taken seriously because of the potential to modify a patient’s lifetime risk of sight threatening sequelae such as myopic maculopathy, cataract, glaucoma and retinal detachment. An earlier age of onset is linked to faster myopic progression, which in turn contributes to increased severity and higher risk of these ocular complications [3–5]. It is commonly held that there is a difference between physiological and pathological myopia, which is arbitrarily defined as 5–6D. However Flitcroft [6] makes the convincing argument that even at 1D of myopia, there is additional pathological risk carried over the emmetrope. Being a low myope of one to three dioptres doubles the odds of myopic maculopathy, triples to quadruples the odds of retinal detachment, and doubles risk of glaucoma and posterior subcapsular cataract [4,6–8] .I’ve been rather pleased with my 1D of myopia over the past 15 years and know I’ll be even more pleased with it in my 40’s, but am wrong to consider it benign. Atrophic myopic maculopathy is a significant cause of blindness in the working population and little advancement has been made in its treatment compared to other ocular pathologies like glaucoma and cataract [6]. Flitcroft’s calculations showed a 60 fold increase in prevalence of myopic maculopathy over 5D compared to lower myopes; even at 3D of myopia, though, there is an almost 10 fold increase in risk. These are startling facts. However it is understandable that the practitioner may not see the lifetime clinical picture of the myope with the risks of paediatric contact lens wear looming in the foreground. Well accepted is the propensity for orthokeratology [9–15] and multifocal soft contact lenses [16–18] to slow progression of myopia. Certainly, the risk of microbial keratitis in contact lens wear is immediate whereas the future risk of glaucoma, or retinal detachment following cataract surgery, does not sit top of mind with a paediatric patient. The evidence, though, demands a long-sighted focus in paediatric myopia management. The incidence of ulcerative keratitis in the non contact lens wearing population is 0.014%, and 0.131% in the contact lens wearing population [19]. By comparison, glaucoma incidence is 4.2% in low myopia (1–3D) and 4.4% in eyes over 3D [4]. Retinal detachment after cataract surgery has an incidence of 1.69% in high myopia [20], and 4.6% after prior repair or retinal breaks or detachment [21], which is more likely in the myope. Comparison
http://dx.doi.org/10.1016/j.clae.2014.05.004 1367-0484/© 2014 British Contact Lens Association. Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Johnson KL. Are we myopic about myopia control? Contact Lens Anterior Eye (2014), http://dx.doi.org/10.1016/j.clae.2014.05.004
G Model CLAE-703; No. of Pages 3
ARTICLE IN PRESS Editorial / Contact Lens & Anterior Eye xxx (2014) xxx–xxx
2
of these percentages paints a convincing picture for our paediatric low myope considering contact lens wear – he or she is 32 times more likely to suffer glaucoma than microbial keratitis. If we can keep a 1D myope out of the next effective risk bracket of 3D, this will mean a reduction in risk odds by 4–5 times for myopic maculopathy, three times for retinal detachment and one and a half times for posterior subcapsular cataract [6]. If this myope instead reaches 5D, they are still 12 times more likely to suffer retinal detachment than contact lens related microbial keratitis. The latter debunks the ‘why bother’ argument of myopia control. The ‘who’ is still unanswered – I understand my clinical colleagues’ hesitation in applying scientific myopia control results to clinical practice. Application of research outcomes to different age and ethnic groups in clinical practice is problematic. Some percentage of children still progress significantly, despite intervention [22]. Most myopia control studies are of one to two years duration, and longer studies have generally shown diminishing results. Percentage rates of myopia control can be difficult to understand. While methodologically sound, an impressive percentage can sometimes translate to 0.25D/year less progression which is clinically unimpressive. We are also yet to find the answer to preventing myopia – an at-risk child must wait for time to take its course and myopia to take hold before we can apply myopia control therapy. We have some understanding of pre-myopia risks, such as family history, binocular vision function, environmental influence and peripheral optics, but all suffer conjecture. Brennan levelled the playing field through evidence that reducing the progression of myopia by 33% would result in a 73% reduction in the frequency of myopia over 5D, and if progression was reduced by 50% this would mean 90% less high myopia [23]. While ‘pathological’ myopia is earnestly regarded, Flitcroft argues that there may be no ‘physiological’ level of myopia where safety of ocular health is outweighed by the minimal benefits of low myopia [6]. Has the time arrived to consider fitting contact lenses for myopia control as a medical necessity, as for keratoconus or aphakia? What further evidence do we need? 2. The clinical myopia profile In the past I found myself having lengthy conversations with parents of myopic children about risk factors for progression, and mechanisms of myopia control. Covering a vast array of literature verbally often resulted in blank stares and a late appointment schedule. In response I developed a Clinical Myopia Profile, which is a communication tool collating a paediatric patient’s risk factors for both myopia development and progression in view of the scientific literature. While best constructed from the individual practitioner’s own understanding and methods of explanation, colleagues around the world have responded favourably to my attempt at synthesising the scientific literature into clinical information, and I have been happy to share it. A child’s binocular vision status, age and refraction, family history, visual tasks, home and leisure environment, and capabilities with modality options must all be considered in profiling myopia. Any parental history of myopia should be an initial trigger to evaluate binocular vision risk factors in the emmetropic child and determine any state of pre-myopia, including lesser levels of paediatric age-normal hyperopia [24]. While there is conjecture [25], managing esophoria and accommodative lag [26–28], and providing advice on environmental risk factors [29], is the limit of evidence-based myopia management for at-risk emmetropes at this point in time. Because of the evidence that there may be no ‘safe’ level of myopia which could be considered physiological, it may not demonstrate best practice clinical care to wait until a child demonstrates consistent progression before commencing myopia control
contact lens wear. Lower levels of myopia which may not traditionally indicate a lifestyle need for contact lens wear, such as the 1D myope without sport participation concerns, should also be considered for active myopia management. Clinical conundrums still exist for the stable paediatric myope; the astigmatic myope where both multifocal and OK visual outcomes may be compromised; the child with severe binocular vision issues who does not achieve control with contact lenses alone; partial correction for higher myopes [30]; children who are contraindicated for contact lens wear; and patients with anatomical limitations for contact lens wear such as East Asian eyelid anatomy affecting OK lens centration. Myopia control is important beyond the lifestyle benefits of contact lens wear and the feelgood factor of a lower prescription – reduction of future ocular health risk is paramount. These risks of myopic maculopathy, glaucoma, retinal detachment and cataract are frequently greater than the risk of serious contact lens complications, and it is crucial to spread the word on this account. Determination of clinical management pathways for myopia are desired, and should remain a hot topic over the coming years, as mechanisms of myopia control are further revealed and novel methods emerge. A combined approach will be required to tackle the unanswered scientific questions and the clinical conundrums, and to then ensure education of young myopes and their parents towards better patient outcomes. References [1] Morgan PB, Efron N. A decade of contact lens prescribing trends in the United Kingdom (1996–2005). Cont Lens Anterior Eye 2006;29:59–68. [2] Efron N, Morgan PB, Woods CA. International survey of rigid contact lens fitting. Optom Vis Sci 2013;90:113–8. [3] Saw S-M, Gazzard G, Shih-Yen EC, Chua W-H. Myopia and associated pathological complications. Ophthal Physiol Opt 2005;25:381–91. [4] Mitchell P, Hourihan F, Sandbach J, Wang JJ. The relationship between glaucoma and myopia: the Blue Mountains Eye Study. Ophthalmology 1999;106:2010–5. [5] Lin LL-K, Shih Y-F, Tsai C-B, Chen C-Y, Lee L-A, Hung P-T, et al. Epidemiologic study of ocular refraction among schoolchildren in Taiwan in 1995. Optom Vis Sci 1999;76:275–81. [6] Flitcroft DI. The complex interactions of retinal, optical and environmental factors in myopia aetiology. Prog Retin Eye Res 2012;31:622–60. [7] Vongphanit J, Mitchell P, Wang JJ. Prevalence and progression of myopic retinopathy in an older population. Ophthalmology 2002;109:704–11. [8] Li X. Incidence and epidemiological characteristics of rhegmatogenous retinal detachment in Beijing, China. Ophthalmology 2003;110:2413–7. [9] Cho P, Cheung SW, Edwards M. The Longitudinal Orthokeratology Research in Children (LORIC) in Hong Kong: a pilot study on refractive changes and myopic control. Curr Eye Res 2005;30:71–80. [10] Walline JJ, Jones LA, Sinnott LT. Corneal reshaping and myopia progression. Br J Ophthalmol 2009;93:1181–5. [11] Swarbrick HA, Alharbi A, Watt K, Lum E. Overnight orthokeratology lens wear slows axial eye growth in myopic children. Invest Ophthalmol Vis Sci 2010;51:1721. [12] Kakita T, Hiraoka T, Oshika T. Influence of overnight orthokeratology on axial elongation in childhood myopia. Invest Ophthalmol Vis Sci 2011;52:2170–4. [13] Cho P, Cheung S-W. Orthokeratology for slowing myopic progression: a randomised controlled trial. Cont Lens Anterior Eye 2011;34:S2–3. [14] Hiraoka T, Kakita T, Okamoto F, Takahashi H, Oshika T. Long-term effect of overnight orthokeratology on axial length elongation in childhood myopia: a 5-year follow-up study. Invest Ophthalmol Vis Sci 2012;53:3913–9. [15] Charm J, Cho P. High myopia-partial reduction ortho-k: a 2-year randomized study. Optom Vis Sci 2013;90:530–9. [16] Anstice NS, Phillips JR. Effect of dual-focus soft contact lens wear on axial myopia progression in children. Ophthalmology 2011;118:1152–61. [17] Sankaridurg P, Holden B, Smith 3rd E, Naduvilath T, Chen X, de la Jara P, et al. Decrease in rate of myopia progression with a contact lens designed to reduce relative peripheral hyperopia: one-year results. Invest Ophthalmol Vis Sci 2011;52:9362–7. [18] Walline JJ, Greiner KL, McVey ME, Jones-Jordan LA. Multifocal contact lens myopia control. Optom Vis Sci 2013;90:1207–14. [19] Jeng BH, Gritz DC, Kumar AB, Holsclaw DS, Porco TC, Smith SD, et al. Epidemiology of ulcerative keratitis in Northern California. Arch Ophthalmol 2010;128:1022–8. [20] Fan DS, Lam DS, Li KK. Retinal complications after cataract extraction in patients with high myopia. Ophthalmology 1999;106:688–91 [discussion 91–2]. [21] Grand MG. The risk of a new retinal break or detachment following cataract surgery in eyes that had undergone repair of phakic break or detachment: a hypothesis of a causal relationship to cataract surgery. Trans Am Ophthalmol Soc 2003;101:335–69.
Please cite this article in press as: Johnson KL. Are we myopic about myopia control? Contact Lens Anterior Eye (2014), http://dx.doi.org/10.1016/j.clae.2014.05.004
G Model CLAE-703; No. of Pages 3
ARTICLE IN PRESS Editorial / Contact Lens & Anterior Eye xxx (2014) xxx–xxx
[22] Chan KY, Cheung SW, Cho P. Orthokeratology for slowing myopic progression in a pair of identical twins. Cont Lens Anterior Eye 2014;37: 116–9. [23] Brennan NA. Predicted reduction in high myopia for various degrees of myopia control. Cont Lens Anterior Eye 2012;35S1:e14–5. [24] Mutti DO, Hayes JR, Mitchell GL, Jones LA, Moeschberger ML, Cotter SA, et al. Refractive error, axial length, and relative peripheral refractive error before and after the onset of myopia. Invest Ophthalmol Vis Sci 2007;48:2510–9. [25] Mutti DO, Mitchell GL, Hayes JR, Jones LA, Moeschberger ML, Cotter SA, et al. Accommodative lag before and after the onset of myopia. Invest Ophthalmol Vis Sci 2006;47:837–46. [26] Nakatsuka C, Hasebe S, Nonaka F, Ohtsuki H. Accommodative lag under habitual seeing conditions: comparison between myopic and emmetropic children. Jpn J Ophthalmol 2005;49:189–94. [27] Gwiazda J, Grice K, Thorn F. Response AC/A ratios are elevated in myopic children. Ophthalmic Physiol Opt 1999;19:173–9.
3
[28] Gwiazda J, Thorn F, Held R. Accommodation, accommodative convergence, and response AC/A ratios before and at the onset of myopia in children. Optom Vis Sci 2005;82:273–8. [29] Rose KA, Morgan IG, Ip J, Kifley A, Huynh S, Smith W, et al. Outdoor activity reduces the prevalence of myopia in children. Ophthalmology 2008;115:1279–85. [30] Charm J, Cho P. High myopia-partial reduction orthokeratology (HM-PRO): study design. Cont Lens Anterior Eye 2013;36:164–70.
Kate L. Johnson (BAppSc(Optom)Hons, GCOT, FBCLA, FIACLE, FCCLSA, FAAO) Gerry & Johnson Optometrists, Level 4, 217 George Street, Brisbane, QLD 4000, Australia E-mail address: [email protected]
Please cite this article in press as: Johnson KL. Are we myopic about myopia control? Contact Lens Anterior Eye (2014), http://dx.doi.org/10.1016/j.clae.2014.05.004