Myopia is the commonest ocular abnormality but as a research topic remains at the margins of mainstream ophthalmology. The concept that most myopes fall into the category of ‘physiological myopia’ ...undoubtedly contributes to this position. Yet detailed analysis of epidemiological data linking myopia with a range of ocular pathologies from glaucoma to retinal detachment demonstrates statistically significant disease association in the 0 to −6 D range of ‘physiological myopia’. The calculated risks from myopia are comparable to those between hypertension, smoking and cardiovascular disease. In the case of myopic maculopathy and retinal detachment the risks are an order of magnitude greater. This finding highlights the potential benefits of interventions that can limit or prevent myopia progression.
Our understanding of the regulatory processes that guide an eye to emmetropia and, conversely how the failure of such mechanisms can lead to refractive errors, is certainly incomplete but has grown enormously in the last few decades. Animal studies, observational clinical studies and more recently randomized clinical trials have demonstrated that the retinal image can influence the eye’s growth. To date human intervention trials in myopia progression using optical means have had limited success but have been designed on the basis of simple hypotheses regarding the amount of defocus at the fovea.
Recent animal studies, backed by observational clinical studies, have revealed that the mechanisms of optically guided eye growth are influenced by the retinal image across a wide area of the retina and not solely the fovea. Such results necessitate a fundamental shift in how refractive errors are defined. In the context of understanding eye growth a single sphero-cylindrical definition of foveal refraction is insufficient. Instead refractive error must be considered across the curved surface of the retina. This carries the consequence that local retinal image defocus can only be determined once the 3D structure of the viewed scene, off axis performance of the eye and eye shape has been accurately defined. This, in turn, introduces an under-appreciated level of complexity and interaction between the environment, ocular optics and eye shape that needs to be considered when planning and interpreting the results of clinical trials on myopia prevention.
We provide a standardized set of terminology, definitions, and thresholds of myopia and its main ocular complications.
Critical review of current terminology and choice of myopia thresholds was done ...to ensure that the proposed standards are appropriate for clinical research purposes, relevant to the underlying biology of myopia, acceptable to researchers in the field, and useful for developing health policy.
We recommend that the many descriptive terms of myopia be consolidated into the following descriptive categories: myopia, secondary myopia, axial myopia, and refractive myopia. To provide a framework for research into myopia prevention, the condition of "pre-myopia" is defined. As a quantitative trait, we recommend that myopia be divided into myopia (i.e., all myopia), low myopia, and high myopia. The current consensus threshold value for myopia is a spherical equivalent refractive error ≤ -0.50 diopters (D), but this carries significant risks of classification bias. The current consensus threshold value for high myopia is a spherical equivalent refractive error ≤ -6.00 D. "Pathologic myopia" is proposed as the categorical term for the adverse, structural complications of myopia. A clinical classification is proposed to encompass the scope of such structural complications.
Standardized definitions and consistent choice of thresholds are essential elements of evidence-based medicine. It is hoped that these proposals, or derivations from them, will facilitate rigorous, evidence-based approaches to the study and management of myopia.
Background Few studies have reported the visual outcomes of small-incision lenticule extraction (SMILE) and laser-assisted subepithelial keratomileusis (LASEK) for myopia correction. This study aims ...to compare the visual quality and corneal wavefront aberrations after SMILE and LASEK for low-myopia correction. Methods In this prospective study, we included 29 eyes of 29 patients who received SMILE and 23 eyes of 23 patients who received LASEK between June 2018 and January 2019. The following measurements were assessed: uncorrected (UDVA) and corrected (CDVA) distance visual acuity, manifest refraction, corneal wavefront aberrations, and subjective visual quality. All patients were followed up for two years. Results All procedures were uneventful. An efficacy index of 1.19 + or - 0.17 was established in the SMILE group and 1.23 + or - 0.20 in the LASEK group. No eyes lost more than two lines of CDVA. We found that 93% (27/29) of the treated eyes in the SMILE group and 91% (21/23) in the LASEK group had spherical equivalent (SE) within + or - 0.25D. The increases in the total corneal spherical aberration and the corneal front spherical aberration were lower in the SMILE group than in the LASEK group (P < 0.01). In contrast, the increases in the total corneal vertical coma and the corneal front vertical coma in the SMILE group were greater than those in the LASEK group (P < 0.01). Conclusion Both SMILE and LASEK have good safety, stability, and patient-reported satisfaction for low myopia. SMILE induced less corneal spherical aberration but greater vertical coma than LASEK. Keywords: Small incision lenticule extraction (SMILE), Laser assisted subepithelial keratomileusis (LASEK), Myopia, Visual quality
The epidemics of myopia: Aetiology and prevention Morgan, Ian G.; French, Amanda N.; Ashby, Regan S. ...
Progress in retinal and eye research,
January 2018, 2018-01-00, 20180101, Letnik:
62
Journal Article
Recenzirano
Odprti dostop
There is an epidemic of myopia in East and Southeast Asia, with the prevalence of myopia in young adults around 80–90%, and an accompanying high prevalence of high myopia in young adults (10–20%). ...This may foreshadow an increase in low vision and blindness due to pathological myopia. These two epidemics are linked, since the increasingly early onset of myopia, combined with high progression rates, naturally generates an epidemic of high myopia, with high prevalences of “acquired” high myopia appearing around the age of 11–13. The major risk factors identified are intensive education, and limited time outdoors. The localization of the epidemic appears to be due to the high educational pressures and limited time outdoors in the region, rather than to genetically elevated sensitivity to these factors. Causality has been demonstrated in the case of time outdoors through randomized clinical trials in which increased time outdoors in schools has prevented the onset of myopia. In the case of educational pressures, evidence of causality comes from the high prevalence of myopia and high myopia in Jewish boys attending Orthodox schools in Israel compared to their sisters attending religious schools, and boys and girls attending secular schools. Combining increased time outdoors in schools, to slow the onset of myopia, with clinical methods for slowing myopic progression, should lead to the control of this epidemic, which would otherwise pose a major health challenge. Reforms to the organization of school systems to reduce intense early competition for accelerated learning pathways may also be important.
•There is an epidemic of myopia in the developed countries of East and Southeast Asia.•A related epidemic of high myopia is due to early onset myopia and rapid myopic progression.•There is a new and highly prevalent form of high myopia, which is acquired rather than genetic.•Intense education and limited time outdoors play major causal roles in both epidemics.•These modifiable risk factors are already being used in schools to contain the epidemics.
I review the key findings and our current knowledge of the cause of myopia, making the connections among the reliable observations on myopia development and theory to arrive at a summary of what we ...know about myopia, the proposed prevailing theory, and applicable action.
Myopia is reaching epidemic proportions. It is estimated that half of the world's population will be myopic by 2050 unless new strategies to fight myopia are developed. Our high-level mathematical description of myopia is translated into clinical applications involving effective treatment and prevention.
A regulating mechanism controlling the refraction of the eye is intimately related to myopia. The approach at hand is to review our knowledge about emmetropization, connecting myopia and emmetropization feedback theory to unveil the cause of myopia.
Many observations discussed here test the validity of feedback theory positively. The cause of human myopia fits perfectly with the idea that emmetropization, in particular its feedback theory implementation, is the controlling mechanism behind myopia. They include near work, atropine, lenses, defocus, and outdoor versus indoor activities. The key findings in myopia research point the same way: myopia is the result of corrective lenses interfering with emmetropization.
We have enough knowledge to answer the question of whether myopia can be reversed or prevented. There is no need to have mathematical skills to apply theory to real cases. It is enough to know the predictions of the feedback theory of emmetropization.
IMPORTANCE: Pathologic myopia due to an excessive increase of axial length is associated with severe visual impairments. Systematic analyses to determine the rate of and the risk factors associated ...with the axial elongation in adults with high myopia based on long-term follow-up of a large population are needed. OBJECTIVE: To determine the risk factors associated with axial elongation in adults with high myopia. DESIGN, SETTING, AND PARTICIPANTS: This cohort study used the medical records of 43 201 patient visits in a single-hospital database that were collected from January 3, 2011, to December 28, 2018. A total of 15 745 medical records with the patients’ sex, best-corrected visual acuity (BCVA), axial length, type of myopic maculopathy, and the presence or absence of choroidal neovascularization (CNV) were reviewed. Data were analyzed from April 3, 2019, to August 5, 2020. MAIN OUTCOMES AND MEASURES: Changes in the axial length at each examination were calculated. The significance of the associations between the annual increase of the axial length and age, sex, baseline axial length, types of myopic maculopathy, and a history of CNV was determined. Generalized linear mixed models were used to evaluate the strength of the risk factors associated with an increase of the axial length in high myopia. RESULTS: Among 1877 patients with 9161 visits included in the analysis, the mean (SD) age was 62.10 (12.92) years, and 1357 (72.30%) were women. The mean (SD) axial length was 29.66 (2.20) mm with a mean (SD) growth rate of 0.05 (0.24) mm/y. Among the 9161 visits, 7096 eyes (77.46%) had myopic maculopathy and 2477 eyes (27.04%) had CNV. The odds ratio for inducing a severe elongation of the axial length was 1.46 (95% CI, 1.38-1.55) for female sex, 0.44 (95% CI, 0.35-0.56) to 0.63 (95% CI, 13 0.50-0.78) for older than 40 years, 1.33 (95% CI, 1.15-1.54) for BCVA of less than 20/400, 1.67 (95% CI, 1.54-1.81) to 2.67 (95% CI, 2.46-2.88) for baseline axial length of 28.15 mm or greater, 1.06 (95% CI, 0.96-1.17) to 1.39 (95% CI, 1.24-1.55) for the presence of maculopathy, and 1.37 (95% CI, 1.29-1.47) for prior CNV. CONCLUSIONS AND RELEVANCE: This cohort study found continuing axial elongation in adults with high myopia. The risk factors for elongation do not appear to be modifiable, so prevention of myopia may be the best approach to reduce the incidence of pathologic myopia and its complications in the future.
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