- •Contents
- •Foreword
- •Dedication
- •Message
- •About the Editors
- •List of Contributors
- •Acknowledgments
- •Introduction
- •Methodologic Issues
- •Review of Studies (Table 1)
- •Cohort Effects on Myopia
- •Risk Factors for Myopia
- •Near work
- •Education/Income
- •Outdoor activity
- •Race/Ethnicity
- •Nuclear cataract
- •Family aggregation/Genetics
- •Siblings
- •Parent-child
- •Other family members
- •Genetics
- •Comments
- •Acknowledgments
- •References
- •Introduction
- •Definition of Myopia in Epidemiologic Studies
- •Risk Factors for Myopia and Ocular Biometry
- •Family history of myopia
- •Near work
- •Outdoor activity
- •Stature
- •Birth parameters
- •Smoking history
- •Breastfeeding
- •Conclusion
- •References
- •Introduction
- •Aetiological Heterogeneity of Myopia
- •Clearly genetic forms of myopia
- •School or acquired myopia
- •Misunderstandings of Heritability and Twin Studies
- •But Heritability has Its Uses
- •Evidence for Genetic Associations of School Myopia
- •Evidence for the Impact of Environmental Factors on Myopia Phenotypes
- •Gene-Environment Interactions and Ethnicity
- •Gene-Environment Interactions and Parental Myopia
- •Conclusion
- •Acknowledgments
- •References
- •Introduction
- •Economic evaluations
- •Full vs partial evaluations
- •Economic evaluation of myopia
- •The Economic Cost of Myopia: A Burden-of-Disease Study
- •China
- •India
- •Europe
- •Singapore
- •Southeast Asia
- •Africa
- •South America
- •Bangladesh
- •ii. Proportion of myopes paying for correction
- •Uncorrected and undercorrected refractive error, spectacle coverage rate and reasons for spectacles nonwear
- •iii. Amount paid for myopic correction
- •Singapore
- •The burden of myopia
- •Further Directions for Economic Research
- •References
- •Introduction
- •Impact of Myopia in Adults
- •Overall Conclusion
- •Future Studies
- •References
- •Introduction
- •Definition of Pathological Myopia
- •Cataract
- •Glaucoma
- •Myopic Maculopathy
- •Myopic Retinopathy
- •Retinal Detachment
- •Optic Disc Abnormalities
- •References
- •Conclusion
- •Introduction
- •The Association Between Myopia and POAG
- •Information from epidemiological studies
- •Asian populations: Myopia and POAG
- •Myopia in other situations
- •Myopia and ocular hypertension
- •Myopia in angle closure
- •Myopia in Pigment Dispersion Syndrome (PDS)
- •Theories for a Link Between Myopia and POAG
- •Glaucoma Assessment in Myopic Eyes
- •Biometric differences
- •Axial length and CCT
- •Optic disc assessment in myopic eyes
- •Visual fields in myopic eyes
- •Imaging tests and variations with myopia
- •ONH susceptibility to damage
- •The Influence of Myopia on the Clinical Management of the Glaucoma Patient
- •Glaucoma progression and myopia
- •References
- •Posterior Staphyloma
- •Myopic Chorioretinal Atrophy
- •Lacquer Cracks
- •Myopic Choroidal Neovascularization
- •Myopic Foveoschisis
- •Myopic macular hole detachments
- •Lattice degeneration
- •Retinal tears and detachments
- •References
- •Introduction
- •Electroretinography
- •Ganzfeld electroretinography
- •Multifocal electroretinography
- •Assessment of Retinal Function
- •Outer retinal (photoreceptor) function
- •Post-receptoral (bipolar cell) and retinal transmission function
- •Inner retinal function
- •Macular function in myopic retina
- •Effect of Long-Term Atropine Usage on Retinal Function
- •Macular Function Associates with Myopia Progression
- •Factors Associated with ERG Changes in Myopia
- •Conclusion
- •References
- •Introduction
- •Genomic Convergence Using Genomic Content
- •Pathway Analysis
- •Pathway analysis in cancer genomics
- •Pathway analysis in GWAS
- •Non-parametric approaches
- •Parametric approaches
- •P-values combining approaches
- •Conclusion
- •References
- •Introduction
- •Definition of Myopia
- •The Classical Twin Model
- •What is the classical twin model?
- •Historical perspective
- •Statistical approaches
- •Twins, Myopia and Heritability Studies
- •Heritability studies for myopia using twins
- •Limitations of using twins in heritability studies
- •Twins and Myopia — Other Studies
- •The Importance of Twin Registries
- •Concluding Comments
- •Acknowledgments
- •References
- •Introduction
- •Candidate Gene Selection Strategies for Myopia
- •Genes Associated With Myopia-Related Phenotypes
- •The HGF/cMET ligand-receptor axis
- •The collagen family of genes
- •Concluding Remarks
- •Acknowledgments
- •References
- •Introduction
- •Phenotypes for Myopia Genetic Studies
- •Study Design
- •Genotyping and Quality Controls
- •Population Structure
- •Association Tests
- •Correlated Phenotypes
- •Imputation and Meta-Analysis
- •Visualization Tools
- •Drawing Conclusions
- •Acknowledgments
- •References
- •Introduction
- •The Search for Error Signals
- •The blur hypothesis
- •Bidirectional lens-compensation
- •Recovery from ametropia vs. compensation for lenses
- •The complication of the emmetropization end-point
- •Optical aberrations as error signals
- •Other possible visual error signals
- •How Important is Having a Fovea?
- •Mechanisms of Emmetropization
- •Scleral similarities and differences between humans and chickens
- •Retinal signals
- •Glucagon-insulin
- •Retinoic acid
- •Dopamine
- •Acetylcholine
- •Choroidal signals
- •The Role of the Choroid in the Control of Ocular Growth
- •Diurnal rhythms and control of ocular growth
- •Conclusions
- •References
- •Introduction
- •Gross Scleral Anatomy
- •Structural organization of the sclera
- •Cellular content of the sclera
- •Mechanical properties of the sclera
- •Structural Changes to the Sclera in Myopia
- •Development of structural and ultrastructural scleral changes in myopia
- •Scleral pathology and staphyloma
- •Biochemical Changes in the Sclera of Myopic Eyes
- •Structural biochemistry of the sclera in myopia
- •Degradative processes in the sclera of myopic eyes
- •Cellular changes in the sclera in myopia
- •Biomechanical Changes in the Sclera of Myopic Eyes
- •Regulators of scleral myofibroblast differentiation
- •Myofibroblast-extracellular matrix interactions
- •Cellular and matrix contributions to altered scleral biomechanics and myopia
- •Scleral Changes in Myopia are Reversible
- •Eye growth regulation during recovery from induced myopia
- •Summary and Conclusions
- •Acknowledgments
- •References
- •Introduction
- •Spatial Visual Performance and Optical Features of the Eye
- •Axial eye growth and development of refractive state
- •Lens thickness and vitreous chamber depth
- •Corneal radius of curvature
- •Schematic eye data
- •Techniques Currently Available for Myopia Studies in the Mouse, Both for Its Induction and Measurement
- •Devices to induce refractive errors
- •Techniques to measure the induced refractive errors and changes in eye growth
- •Refractive state
- •Corneal radius of curvature
- •Axial length measurements and ocular biometry
- •Measurements of the optical aberrations of the mouse eye
- •Behavioral measurement of grating acuity and contrast sensitivity in the mouse
- •Recent Studies on Myopia in the Mouse Model: Some Examples
- •Magnitudes of experimentally induced refractive errors in wild-type mice
- •Refractive development in mutant mice
- •Pharmacological studies to inhibit axial eye growth in mice
- •Image processing and regulation of retinal genes and proteins
- •Summary
- •Acknowledgments
- •References
- •Introduction
- •A Brief Introduction to Comparative Genomics
- •Comparative Expression
- •Genes in Retina and Sclera in Animal Models of Myopia
- •ZENK (EGR-1)
- •Scleral Gene Expression in a Mouse Model of Myopia
- •RNA, Target cDNA and Microarray Chip Preparation
- •Microarray Data Analysis
- •Scleral Gene Expression in the Myopic Mouse
- •Summary
- •References
- •Introduction
- •Possible Mechanisms of Pharmacological Treatment
- •Efficacy Studies
- •Other Issues Related to Drugs
- •Potential Side Effects
- •The Future of Drug Treatment in Myopia
- •Conclusions
- •References
- •Introduction
- •Accommodation
- •Close work
- •Physical characteristics of the retinal image
- •Visual deprivation
- •Compensatory changes in refraction
- •Intensity and periodicity of light exposure
- •Spatial frequency
- •Light periodicity
- •Image clarity
- •Outdoor activity and retinal image blur
- •Light vergence and photon catch
- •Chromaticity
- •Therapeutic implications
- •References
- •Index
106 Jeganathan et al.
Cataract extraction in high myopia must be considered carefully because patients with high myopia are at increased risk of retinal breaks and retinal detachment.51,52
Glaucoma
An association between high myopia and primary open angle glaucoma (POAG) has been supported by numerous case series, case control, and large population-based studies (Table 2).38,53–61,63 The prevalence of myopia with POAG is 4% and may increase to 6–7% with higher degrees of myopia.62 In the BMES, after adjusting for age, gender and other risk factors, glaucoma was two to three times as frequent as eyes with myopia compared with eyes with emmetropia or hyperopia.55 In the Barbados Eye Study, a myopic refraction was one of several risk factors in adult black people with prevalent POAG.38,63 Both the BMES and Barbados Eye Study confirm a dose-response between the level of myopia and prevalence of glaucoma.38,55,63 Severe myopia (< − 4D), not mild myopia, has been shown to be a significant risk factor for subsequent visual field loss in patients with POAG.64 However, in the Ocular Hypertension Treatment Study, high myopia was not predictive of POAG.65 Moreover, individuals with myopia were not found to have a higher incidence or progression of glaucoma in the Ocular Hypertension Treatment Study or Early Manifest Glaucoma Trial.65,66 High myopia is related with higher intraocular pressure (IOP) and occurs more often in glaucoma patients than in the normal population, particularly amongst the elderly.55 In POAG patients with high IOP, higher myopia is thought to be a factor that threatens their quality of life.67 Interestingly, the visual field of myopic eyes more often improves and less often worsens once the IOP has been lowered therapeutically. There is now evidence that myopia is a risk factor for the development of ocular hypertension, based on data of the screening examination for the Early Manifest Glaucoma Trial and other studies.68–70 Structural changes associated with myopia, such as longer axial length, larger and/or tilted optic disc, thinner lamina cribrosa, peripapillary atrophy, and shared alteration in collagen and other extracellular matrix of the optic nerve is postulated to make the upper maculopapillary bundle (lower cecofield) more susceptible to glaucomatous injury.67 Highly myopic patients are also at higher risk of postoperative hypotony maculopathy.71
Table 2. Summary of Published Data on Myopia and Glaucoma
|
|
|
Study |
Sample |
Age |
|
Definition of |
Summary of Main |
Source |
Year |
Place |
Design |
Size (n) |
(Years) |
Methodology |
Myopia |
Findings |
|
|
|
|
|
|
|
|
|
Daubs and |
1981 |
London, |
CCS |
953 |
≥ 40 |
SR OAG-eyes |
High myopia |
OR of OAG = 3.1 (95% CI 1.6, |
Crick53 |
|
United |
|
|
|
with open |
(≤ −5 D) |
5.8) OR of OAG = 1.3 |
|
|
Kingdom |
|
|
|
angles and |
Low myopia |
(1.0, 1.8). Adjusted for age, |
|
|
|
|
|
|
VFD |
(−0.25 D to |
IOP, sex, family history, blood |
|
|
|
|
|
|
|
−5 D) |
pressure, astigmatism, season, |
|
|
|
|
|
|
|
|
health. |
Ponte et al.; |
1994 |
Italy |
PBCS |
264 |
≥ 40 |
Cases: IOP ≥ 24, |
≤ −0.5 D |
OR of glaucoma prevalence = |
Casteldaccia |
|
|
|
|
|
history of |
|
5.56 (1.85, 16.67). Adjusted for |
Eye Study54 |
|
|
|
|
|
glaucoma, |
|
diabetes, hypertension, |
|
|
|
|
|
|
VFD. Controls: |
|
steroids, iris texture. |
|
|
|
|
|
|
IOP ≤20, |
|
|
|
|
|
|
|
|
CDR 0–0.2 |
|
|
Mitchell et al; |
1999 |
Sydney, |
PBCS |
3654 |
≥ 49 |
AR and SR OAG |
High myopia |
OR of OAG prevalence = |
Blue |
|
Australia |
|
|
|
defined as |
≤ −3 D |
3.3 (1.7, 6.4) OR of OAG |
Mountains |
|
|
|
|
|
CDR ≥0.7 or |
Low myopia |
prevalence = 2.3 (1.3, 4.1). |
Eye Study55 |
|
|
|
|
|
CD asymmetry |
(−3 D to |
Adjusted for gender, family |
|
|
|
|
|
|
≥0.3 |
≥ −1 D) |
history, diabetes, hypertension, |
|
|
|
|
|
|
|
|
migraine, steroid use, |
|
|
|
|
|
|
|
|
psedoexfoliation. |
Wu et al; |
1999 |
Barbados |
PBSC |
4709 |
40–84 |
AR OAG-eyes |
≤ −0.5 D |
OR of OAG prevalence = |
Barbados |
|
|
|
|
|
with open |
|
1.48 (1.12,1.95). |
Eye Study38 |
|
|
|
|
|
angles and VFD |
|
|
(Continued )
Myopia Pathological of Morbidity Ocular 107
|
|
|
|
|
Table 2. |
(Continued ) |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Study |
Sample |
Age |
|
Definition of |
Summary of Main |
Source |
Year |
Place |
Design |
Size (n) |
(Years) |
Methodology |
Myopia |
Findings |
Grodum et al.56 |
2001 |
Malmo, |
PBCS |
32,918 |
57–79 AR OAG defined |
≤ −1 D |
|
|
Sweden |
|
|
as 2 repeatable |
|
|
|
|
|
|
VFD |
|
Yoshida et al.57 |
2001 |
Yokohama, |
CCS |
64,394 |
≥ 49 AR POAG defined |
≤ −3 D |
|
|
Japan |
|
|
as glaucomatous |
|
|
|
|
|
|
VFD associated |
|
|
|
|
|
|
with abnormal |
|
|
|
|
|
|
optic disc |
|
|
|
|
|
|
and/or disc |
|
|
|
|
|
|
margin |
|
Prevalence of newly diagnosed OAG increased with increasing myopia (p < 0.01), and 1.5% in moderate to high myopia. Adjusted for age, gender, IOP.
Prevalence of POAG is higher in moderate to high myopes
(p < 0.001).
Wong et al; |
2003 Wisconsin, PBCS |
4670 43–86 AR and SR POAG ≤ −1 D |
OR of prevalent POAG for |
Beaver Dam |
USA |
defined as |
myopia = 1.6 (1.1, 2.3). |
Eye Study58 |
|
IOP ≥ 22, |
Adjusted for age and gender. |
|
|
CDR ≥ 0.8, VFD, |
|
|
|
history of |
|
|
|
glaucoma |
|
|
|
treatment |
|
|
|
|
|
|
|
|
(Continued ) |
.al et Jeganathan 108
Table 2. (Continued )
|
|
|
Study |
Sample |
Age |
|
Definition of |
Summary of Main |
Source |
Year |
Place |
Design |
Size (n) |
(Years) |
Methodology |
Myopia |
Findings |
|
|
|
|
|
|
|
|
|
Suzuki et al; |
2006 |
Tajimi, |
PBCS |
119 |
≥ 40 |
AR POAG |
Low myopia |
OR of prevalent POAG = |
Tajimi |
|
Japan |
|
|
|
diagnosed from |
(−3 D to −1 D) |
1.85 (1.03, 3.31) for low |
Eye Study59 |
|
|
|
|
|
IOP, CDR, |
Moderate to |
myopia and 2.60 (1.56, 4.35) |
|
|
|
|
|
|
and VFD |
high myopia |
for moderate to high myopia. |
|
|
|
|
|
|
|
(≤ −3 D) |
Adjusted for age, gender, IOP, |
|
|
|
|
|
|
|
|
corneal curvature, central |
|
|
|
|
|
|
|
|
corneal thickness, diabetes, |
|
|
|
|
|
|
|
|
migraine, hypertension, |
|
|
|
|
|
|
|
|
smoking, family history of |
|
|
|
|
|
|
|
|
glaucoma. |
Xu. et al; |
2007 |
Beijing, |
PBCS |
4439 |
≥ 40 AR and SR |
High myopia |
OR of prevalent POAG in highly |
|
Beijing |
|
China |
|
|
|
POAG diagnosed |
(> −8 D) |
myopic marked myopia = |
Eye Study60 |
|
|
|
|
|
from CDR |
Marked myopia |
2.28 (0.99, 5.25) compared to |
|
|
|
|
|
|
(photos) and |
(< −6 D to −8 D) |
moderate myopia. The OR was |
|
|
|
|
|
|
IOP |
Moderate myopia |
significantly higher than in |
|
|
|
|
|
|
|
(< −3 D to −6 D) |
the group with low myopia |
|
|
|
|
|
|
|
|
(OR 3.5; 1.71, 7.25). |
Casson, et al; |
2007 |
Meiktila, |
PBCS |
2076 |
≥ 40 |
AR POAG |
Myopia < 0.5 D |
Myopia (P = 0.049), increasing |
Meiktila |
|
Burma |
|
|
|
diagnosed from |
|
age, and IOP (P < 0.001) were |
Eye Study61 |
|
|
|
|
|
IOP, CDR, and |
|
significant risk factors for |
|
|
|
|
|
|
VFD |
|
POAG. |
Myopia Pathological of Morbidity Ocular 109
AR: autorefraction, CDR: cup-disc ratio, CI: confidence interval, CCS: case control study, D: dioptres, IOP: intraocular pressure, OR: odds ratio, PBSC: pop- ulation-based cross-sectional study, POAG: primary open angle glaucoma, SR: subjective refraction, VFD: visual field defect.
