PATHOLOGIC MYOPIA

Foreword I
Foreword II
Preface
Contents
Contributors
Part I: Basic Science of Pathologic Myopia
	1: Myopia: A Historical Perspective
		1.1	 Pre-ophthalmoscopic Historical Landmarks in Myopia
		1.2	 Post-ophthalmoscopic Historical Landmarks in Myopia (1851)
		1.3	 Modern Historical Landmarks in Myopia
		1.4	 Recent Historical Landmarks in Myopia
		References
	2: Definition of Pathologic Myopia (PM)
		References
	3: Epidemiology of Myopia, High Myopia, and Pathological Myopia
		3.1	 Introduction
		3.2	 East–West Patterns in the Prevalence of Myopia
		3.3	 Prevalence of High Myopia
		3.4	 Prevalence of Pathological Myopia
		3.5	 Associations of Myopia with Other Age-Related Eye Diseases
			3.5.1	 Age-Related Macular Degeneration (AMD)
			3.5.2	 Diabetic Retinopathy (DR)
			3.5.3	 Age-Related Cataract
			3.5.4	 Primary Open-Angle Glaucoma (POAG)
		3.6	 Environmental Risk Factors for Myopia
			3.6.1	 Near Work and Education
			3.6.2	 Screen Time
			3.6.3	 Time Outdoors
		3.7	 Answered and Unanswered Questions
		3.8	 Conclusions
		References
	4: Genetics of Pathologic Myopia
		4.1	 Introduction
		4.2	 Genetic Contribution in Pathologic Myopia
		4.3	 Genetic Loci and Genes Associated with Complex Pathologic Myopia
		4.4	 Genetic Loci and Genes for Nonsyndromic Mendelian Pathologic Myopia
		4.5	 Genes for Syndromic Pathologic Myopia
			4.5.1	 Pathologic Myopia Accompanied with Ocular Diseases
			4.5.2	 Pathologic Myopia Accompanied with Systemic Diseases
		4.6	 Clinical Gene Test for Pathologic Myopia
		4.7	 Perspectives
		References
	5: Public Health Impact of Pathologic Myopia
		5.1	 Epidemiology of Pathologic Myopia (PM)
			5.1.1	 Overview and Definition of PM
			5.1.2	 Prevalence, Incidence, and Progression of PM
			5.1.3	 Risk Factors of PM
		5.2	 Public Health Impact of PM
			5.2.1	 Blindness and VI Associated with PM
			5.2.2	 The Quality of Life (QoL) Impact of PM
		5.3	 Public Health Strategies to Manage the Burden of PM
			5.3.1	 Strategy 1: Health Promotion Programs
				5.3.1.1	 Myopia Prevention and Control
				5.3.1.2	 Public Health Education Campaigns and Regular Screening
			5.3.2	 Strategy 2: Provisions for Treating Complications of PM
				5.3.2.1	 Diagnostics
				5.3.2.2	 Treatment
			5.3.3	 Strategy 3: Low Vision Care and Rehabilitation
		5.4	 Future Direction and Work: Item Banking and Computerized Adaptive Testing in Myopia
		5.5	 Conclusion
		References
	6: Animal Models of Experimental Myopia: Limitations and Synergies with Studies on Human Myopia
		6.1	 Refractive Development and Incident Myopia in Children
		6.2	 Experimental Myopia
			6.2.1	 The Basic Paradigms in Experimental Myopia
				6.2.1.1	 Form-Deprivation Myopia (FDM)
				6.2.1.2	 Lens-Induced Myopia (LIM)
				6.2.1.3	 How Different Are FDM and LIM?
				6.2.1.4	 Recovery from Experimental Myopia (REC)
				6.2.1.5	 Lens-Induced Hyperopia (LIH)
				6.2.1.6	 How Similar Are the REC and LIH Paradigms?
				6.2.1.7	 What Is the Best Model in Terms of Stimulus Relevance to Human Myopia?
				6.2.1.8	 Which Is the Best Species to Study for Relevance to Human Myopia?
		6.3	 Important Features of Experimental Myopia
			6.3.1	 Local Control and Spatial Localisation
			6.3.2	 Choroidal Changes
			6.3.3	 Summary
		6.4	 Synergies Between Genetic Research on Human and Experimental Myopia
		6.5	 Control of the Onset and Progression of Myopia
			6.5.1	 Control of Myopia Progression with Atropine
			6.5.2	 Optical Control of Myopia Progression
			6.5.3	 Is Peripheral Defocus Important?
			6.5.4	 Protective Effects of Time Outdoors
			6.5.5	 Changes in Scleral Metabolism
			6.5.6	 A Heuristic Model of Growth Control
		6.6	 Conclusions
		References
	7: The Sclera and Its Role in Regulation of the Refractive State
		7.1	 Introduction
		7.2	 Development
		7.3	 The Structure of the Sclera
		7.4	 Age-Related Changes in the Sclera
		7.5	 Scleral Changes During Myopia Development
		7.6	 Regulation of Scleral Growth and/or Remodeling
		7.7	 Conclusions
		References
Part II: Ocular Changes in the Development of Pathologic Myopia
	8: Update on the Pathology of Pathological Myopia
		8.1	 Introduction
		8.2	 Pathological Findings in Pathological Myopia
			8.2.1	 Lacquer Cracks
			8.2.2	 Geographic Atrophy of RPE and Choroid (Diffuse Versus Patchy)
			8.2.3	 Posterior Staphyloma
			8.2.4	 CNV/Fuchs Spot
			8.2.5	 Retinal and Macular Hole/Schisis/Detachment
			8.2.6	 Myopic Configuration of the Optic Nerve Head, Including Peripapillary Changes
			8.2.7	 Vitreous Degeneration
		8.3	 Conclusion
		References
	9: The Sclera and Induced Abnormalities in Myopia
		9.1	 Embryology and Development of the Sclera
		9.2	 Gross Scleral Anatomy of an Emmetropic Eye
		9.3	 Fine Anatomy of the Sclera
		9.4	 Mechanical Properties of the Sclera
		9.5	 Emmetropization and Myopization
		9.6	 Human Myopia
		9.7	 Ocular Shape
		9.8	 Shape Alterations Across Smaller Units of Scale
		9.9	 Ectasia of the Sclera and Intrascleral Cavitations Related to Emissary Openings
		9.10	 Irregularities of the Thinned Sclera
		References
	10: The Choroid
		10.1	 The Embryology and Anatomy of the Choroid
			10.1.1 Embryology
			10.1.2 Choroidal Anatomy
		10.2	 Blood Flow Within the Choroid
		10.3	 The Regulation of Choroidal Blood Flow
		10.4	 Other Choroidal Functions
		10.5	 Imaging the Choroid
			10.5.1 Angiography
			10.5.2 Ultrasonography
			10.5.3 Optical Coherence Tomography
				10.5.3.1	 Interferometry
		10.6	 Measurements and Reproducibility of Choroidal Thickness
		10.7	 Normal Subfoveal Choroidal Thickness
		10.8	 Topography of Choroidal Thickness
		10.9	 Imaging the Internal Structure of the Choroid
		10.10	 Optical Coherence Tomography Angiography
		10.11	 The Choroid in High Myopia
		10.12	 Biometric Choroidal Changes and Their Clinical Significance
		10.13	 Chorioretinal Atrophy in High Myopia
		10.14	 Intrachoroidal Cavitation
		10.15	 Focal Choroidal Excavation
		10.16	 Future Trends for Research
			10.16.1 Potential Use of Choroidal Thickness in Grading Myopic Fundus Changes
			10.16.2 Optical Coherence Tomography Angiography
		References
	11: Theories of Myopization: Potential Role of a Posteriorly Expanding Bruch’s Membrane
		11.1	 Introduction
		11.2	 Sclera
		11.3	 Choroid
		11.4	 Bruch’s Membrane (BM)
		11.5	 Macular BM Length and Density of Retinal Pigment Epithelium Cells and Retinal Thickness in the Macular Region and Fundus Periphery
		11.6	 Optic Disc Size and Shape in Myopia
		11.7	 Process of Emmetropization
		References
	12: The Optic Nerve Head in High Myopia/Abnormalities of the Intrapapillary and Parapapillary Region
		12.1	 Intrapapillary Region
			12.1.1	 Optic Disc
			12.1.2	 Neuroretinal Rim
			12.1.3	 Optic Cup
			12.1.4	 Histology of the Intrapapillary Region
		12.2	 Parapapillary Region
			12.2.1	 Parapapillary Atrophy
			12.2.2	 Peripapillary Border Tissue of the Choroid and Peripapillary Scleral Flange
			12.2.3	 Peripapillary Scleral Flange
		References (Further References Are Found in These Citations)
	13: Vitreous Changes in Myopia
		13.1	 Introduction
		13.2	 Anatomy of the Vitreous
			13.2.1	 Embryology of the Vitreous [4]
				13.2.1.1	 Formation of Primary Vitreous (Fourth to Sixth Week; 4–13 mm Stage)
				13.2.1.2	 Formation of Secondary Vitreous (Sixth Week to Third Month; 13–70 mm Stage)
				13.2.1.3	 Late Fetal Development
			13.2.2	 Vitreous Development After Birth
			13.2.3	 Microscopic Anatomy
				13.2.3.1	 The Vitreous Body
			13.2.4	 Vitreoretinal Interface
			13.2.5	 Biomicroscopic Anatomy
			13.2.6	 Posterior Precortical Vitreous Pocket (PPVP)
				13.2.6.1	 Biomicroscopy of Posterior Precortical Vitreous Pocket
				13.2.6.2	 Optical Coherence Tomography of Posterior Precortical Vitreous Pocket
				13.2.6.3	 Clinical Implication of Posterior Precortical Vitreous Pocket
		13.3	 Age-Related Change of the Vitreous
			13.3.1	 Liquefaction
			13.3.2	 Posterior Vitreous Detachment (PVD)
			13.3.3	 Evolution of Vitreomacular Detachment
			13.3.4	 Splitting of Vitreous Cortex
		13.4	 Vitreous Changes in Myopic Eyes
			13.4.1	 Formation of Large Lacuna
			13.4.2	 Incomplete PVD
			13.4.3	 Early PVD
			13.4.4	 Residual Vitreous Cortex in Eyes with Complete PVD
		13.5	 Conclusion
		References
	14: Ultra-widefield Imaging of Vitreous in Pathologic Myopia
		14.1	 Introduction: ‘In Vivo’ Widefield Vitreous Imaging
			14.1.1	 Ultrasonography
			14.1.2	 Optical Coherence Tomography
			14.1.3	 Prototype Widefield Optical Coherence Tomography Instrument
		14.2	 Ultra-widefield OCT Imaging of Vitreous in Pathologic Myopia
			14.2.1	 Early Posterior Vitreous Detachment
			14.2.2	 Asymmetrical Posterior Vitreous Detachment
			14.2.3	 Multiple and Multi-layered Posterior Vitreous Detachment
			14.2.4	 Long Strands of Posterior Vitreous
		14.3	 Relationship Between Posterior Vitreous and Retinal Vessels in Pathologic Myopia
			14.3.1	 Histology; Vitreo-vascular Interface
			14.3.2	 Vitreal Adhesion to Retinal Vessels
			14.3.3	 Paravascular Cystic Lesion, Paravascular Lamellar Hole, and Vascular Microfold
			14.3.4	 Relationship Between Posterior Vitreous and Macular Retinoschisis
		References
Part III: Sequella of Pathologic Myopia and Their Potential Treatments
	15: Staphyloma I
		15.1	 Historical Development of Ideas
		15.2	 Classification
		15.3	 Prevalence of Staphyloma
		15.4	 Proposed Nomenclature
		15.5	 Etiology
		15.6	 Special Problems in High Myopes That Can Be Attributed to Staphylomas
		15.7	 Localized Retinal Detachment Over a Staphyloma
		15.8	 Ocular Alignment Problems
		15.9	 Visual Field Abnormalities
		15.10	 Dome-Shaped Macula and Allied Disorders
		15.11	 Potential Mechanisms of Serous Detachment in Staphyloma and Dome-Shaped Macula
		References
	16: Staphyloma II: Morphological Features of Posterior Staphyloma in Pathologic Myopia – Analysis Using 3D MRI and Ultra-widefield OCT
		16.1	 Introduction
		16.2	 Detection of Staphyloma Edges by Ultra-widefield OCT
			16.2.1 Highly Myopic Eyes Without Evident Staphyloma (Fig. 16.4)
		16.3	 Highly Myopic Eyes with Evident Staphyloma (Figs. 16.6, 16.7, 16.8, 16.9, 16.10, 16.11, and 16.12)
		16.4	 Macular Staphyloma
		16.5	 Wide, Macular Staphyloma (Fig. 16.6)
		16.6	 Narrow, Macular Staphyloma (Fig. 16.8)
		16.7	 Inferior Staphyloma (Fig. 16.10)
		16.8	 Peripapillary Staphyloma (Fig. 16.11)
		16.9	 Nasal Staphyloma (Fig. 16.13)
		16.10	 Others
			16.10.1 Peripapillary, Wide
			16.10.2 Comments
		References
	17: Myopic Maculopathy
		17.1	 Introduction
		17.2	 Features of Each Lesion of Myopic Maculopathy
			17.2.1	 Tessellated (or Tigroid) Fundus
			17.2.2	 Lacquer Cracks
			17.2.3	 Diffuse Choroidal Atrophy
			17.2.4	 Patchy Chorioretinal Atrophy
			17.2.5	 Others
				17.2.5.1	 Macular Lesions in Dome-Shaped Macula
			17.2.6	 Macular Lesions Along the Edge of Tilted Disc Syndrome
		17.3	 Frequency of Myopic Maculopathy
		17.4	 Progression of Myopic Maculopathy
		17.5	 Factors Correlating with the Development of Myopic Maculopathy
		17.6	 Future Perspective
		References
	18: Overview of OCT-Based Classification of Macular Lesions Due to Pathologic Myopia
		18.1	 Introduction
		18.2	 META-PM Classification of Myopic Maculopathy (Table 18.1) [26]
			18.2.1	 The Details of META-PM and Several Supplements for Myopic Maculopathy
			18.2.2	 Why the OCT-Based Classification Is Needed?
		18.3	 OCT Features of Each Lesion of Myopic Maculopathy
			18.3.1	 Choroidal Thinning
			18.3.2	 Bruch’s Membrane Holes
			18.3.3	 Other Myopic Lesions (Myopic Traction Maculopathy and Dome-Shaped Macula)
		18.4	 Establishment of OCT-Based Classification
			18.4.1	 Choroidal Thickness Profile in Each Lesion
				18.4.1.1	 Profile in Myopic Maculopathy Is Different from Normal Fundus
				18.4.1.2	 Progressive Thinning from Tessellated to PDCA and to MDCA, but Not Thereafter
			18.4.2	 Cut-Off Value of Choroidal Thickness for Identifying PDCA and MDCA
		18.5	 Summary of OCT-Based Classification of Myopic Maculopathy (Table 18.2)
		18.6	 A Scheme Depicting the Progression Patterns of Myopic Maculopathy Combining with OCT Finding (Fig. 18.7)
		18.7	 Future Perspective
		References
	19: Choroidal Neovascularization
		19.1	 Background
		19.2	 Clinical Characteristics
		19.3	 Potential Pathologic Mechanisms
		19.4	 Disease Characteristics
		19.5	 Treatment of Myopic Choroidal Neovascularization
		19.6	 Thermal Laser Photocoagulation
		19.7	 Laser Photocoagulation for Myopic Choroidal Neovascularization
		19.8	 Surgical Treatment
		19.9	 Photodynamic Therapy
		19.10	 Agents Directed Against Vascular Endothelial Growth Factor
		19.11	 Recommended Treatment of Eyes with Myopic Choroidal Neovascularization
		19.12	 Retinal Pigment Epithelial Loss and Atrophy
		References
	20: Myopic Macular Retinoschisis
		20.1	 Myopic Macular Retinoschisis and Associated Lesions
		20.2	 Clinical Features of MRS
		20.3	 Diagnosis of MRS
		20.4	 Pathological Findings of MRS
		20.5	 Factors Related to MRS Development
		20.6	 Natural Course
		20.7	 Treatment for MRS
		20.8	 Other Types of Macular Retinal Detachments in Pathologic Myopia
			20.8.1	 Macular Hole Retinal Detachment (MHRD)
			20.8.2	 Macular RD Associated with Peripapillary Intrachoroidal Cavitation (ICC)
			20.8.3	 RD Caused by a Retinal Break in and Along the Macular Atrophy or Patchy Atrophy
		20.9	 Closing Remarks
		References
	21: Surgical Approaches for Complications of PM
		21.1	 Indication for Surgery
			21.1.1	 Introduction and Definitions
			21.1.2	 Indications for Surgery
				21.1.2.1	 Myopic Traction Maculopathy
				21.1.2.2	 Full-Thickness Macular Hole
				21.1.2.3	 Retinal Detachment with a Macular Hole
		21.2	 Surgical Procedures
			21.2.1	 Vitrectomy
			21.2.2	 Posterior Hyaloid Detachment
			21.2.3	 Epiretinal Membrane Peeling
			21.2.4	 Internal Limiting Membrane Peeling
			21.2.5	 Other Procedures
		21.3	 Intraoperative and Postoperative Complications
			21.3.1	 Intraoperative Complications
			21.3.2	 Postoperative Complications
		21.4	 Usefulness of Intraoperative OCT
		References
	22: Peripheral Retinal Abnormalities
		22.1	 Introduction
		22.2	 Lattice Degeneration
			22.2.1	 Historical Background
			22.2.2	 Clinical Features
			22.2.3	 Prevalence
			22.2.4	 Clinical Variants
				22.2.4.1	 Snail-Track Degeneration
			22.2.5	 Associations with Hereditary Disorders
			22.2.6	 Histologic Features
			22.2.7	 Pathogenesis
			22.2.8	 Evolution and Management
		22.3	 White-Without-Pressure
			22.3.1	 Clinical Features
			22.3.2	 Prevalence
			22.3.3	 Pathogenesis and Histology
			22.3.4	 Evolution and Prognosis
			22.3.5	 Associations and Variants
				22.3.5.1	 Associations
				22.3.5.2	 Dark-Without-Pressure
		22.4	 Pigmentary Degeneration
			22.4.1	 Clinical Features
			22.4.2	 Prevalence
			22.4.3	 Pathogenesis and Evolution
			22.4.4	 Differential Diagnosis
		22.5	 Paving Stone Degeneration (Cobblestone Degeneration)
			22.5.1	 Clinical Features
			22.5.2	 Prevalence
			22.5.3	 Histologic Features and Pathogenesis
			22.5.4	 Evolution
		22.6	 Retinal Breaks
			22.6.1	 Prevalence
		22.7	 Tractional Retinal Tears
			22.7.1	 Clinical Features and Classification
			22.7.2	 Giant Tear
			22.7.3	 Iatrogenic Retinal Tears
		22.8	 Atrophic Retinal Holes
		22.9	 Risk of Retinal Detachment and Prophylactic Therapy of Retinal Breaks
			22.9.1	 Modulation of the Risk in Myopic, Aphakic, and Fellow Eyes
		References
	23: Retinal Detachment
		23.1	 Introduction
		23.2	 The Myopic Eye: Features Predisposing to Retinal Detachment
			23.2.1	 Alterations in the Myopic Vitreous Gel
			23.2.2	 Vitreous Liquefaction and Myopia
			23.2.3	 Posterior Vitreous Detachment (PVD)
			23.2.4	 Vitreoretinal Adhesions Associated with Peripheral Vitreoretinal Degenerative Disorders
			23.2.5	 Visible Vitreoretinal Adhesions
			23.2.6	 Invisible Vitreoretinal Adhesions
		23.3	 Prevention of Rhegmatogenous Retinal Detachment in Myopia
			23.3.1	 Treatment of Visible Vitreoretinal Adhesions in Myopia
			23.3.2	 Treatment of Invisible Vitreoretinal Adhesions in Myopia
		23.4	 Treatment of Rhegmatogenous Retinal Detachment in Myopia
			23.4.1	 Surgery for Uncomplicated Myopic RRDs with Peripheral Retinal Breaks
			23.4.2	 Scleral Buckling
			23.4.3	 Advantages
			23.4.4	 Disadvantages
			23.4.5	 Vitrectomy
			23.4.6	 Advantages
			23.4.7	 Disadvantages
			23.4.8	 Pneumatic Retinopexy
			23.4.9	 Advantages
			23.4.10	 Disadvantages
			23.4.11	 Surgery for Myopic RRDs with Posterior Retinal Breaks
			23.4.12	 Pneumatic Procedures for Myopic RRDs Due to Macular Holes
			23.4.13	 Vitrectomy for Myopic RRDs Due to Macular Holes
			23.4.14	 Scleral Buckling for Myopic RRDs Due to Macular Holes
		23.5	 Conclusions
		References
	24: Glaucoma in Myopia
		24.1	 Introduction
		24.2	 Myopia as a Risk Factor for Open-Angle Glaucoma
		24.3	 Diagnosis and Monitoring of Glaucoma in Myopia: Optic Nerve Structure
		24.4	 Diagnosis and Monitoring of Glaucoma in Myopia: Optic Nerve Function
		24.5	 Treatment of Glaucoma in Myopia
		24.6	 Conclusions
		References
	25: Myopic Optic Neuropathy
		25.1	 Embryology of the Optic Nerve
		25.2	 Anatomy of the Optic Nerve
		25.3	 Morphometric Characteristics of the Optic Disc in Normal Eyes
		25.4	 Optic Nerve Hypoplasia
		25.5	 Glaucoma
		25.6	 Optic Neuropathies Associated with High Myopia
			25.6.1	 Overview
		25.7	 Tilted Discs
		25.8	 Optic Neuropathy Associated with Optic Nerve Abnormalities That May Not Be Progressive
		25.9	 Optic Disc Abnormalities Associated with Generalized Expansion
			25.9.1	 Dilation of Perioptic Subarachnoid Space and Thinning of Peripapillary Sclera
			25.9.2	 Formation of Acquired Pits in the Optic Disc and Conus Regions
			25.9.3	 Separation of Circle of Zinn-Haller from the Optic Nerve
		25.10	 Eye Shape Abnormalities
		25.11	 Myopic Optic Neuropathy
		25.12	 The Need for Future Research
		References
	26: Special Considerations for Cataract Surgery in the Face of Pathologic Myopia
		26.1	 Introduction
		26.2	 Epidemiology
		26.3	 Pathogenesis
		26.4	 Preoperative Planning
			26.4.1	 Axial Length and Keratometry
			26.4.2	 Intraocular Lens Power Calculation
			26.4.3	 Intraocular Lens Options
			26.4.4	 Expectations
		26.5	 Timing Considerations
		26.6	 Anesthesia
		26.7	 Surgical Considerations
		26.8	 Postoperative Management
		26.9	 Conclusion
		References
	27: Ocular Motility Abnormalities
		27.1	 Highly Myopic Strabismus
			27.1.1	 Etiology
			27.1.2	 Angle of Dislocation
			27.1.3	 Surgical Treatment
			27.1.4	 Surgical Options
			27.1.5	 Dynamic Changes of Globe Dislocation
		27.2	 Myopia and Concomitant Strabismus
		References
	28: Myopia: Ocular and Systemic Disease
		28.1	 Introduction
		28.2	 Myopia in Association with Ocular Diseases
			28.2.1	 High Myopia Associated with Form-Depriving Ocular Conditions
			28.2.2	 High Myopia Associated with Ocular Disorders of Connective Tissue
			28.2.3	 Other Ocular Disorders That Associate with Myopia
		28.3	 Myopia Associated with Systemic Diseases and Syndromes
		28.4	 Drug-Induced Myopia
			28.4.1	 Proposed Mechanisms of Drug-Induced Myopia
			28.4.2	 Differentiating Between Mechanisms
			28.4.3	 Drugs Reported to Induce Myopia
				28.4.3.1	 Sulfonamides
				28.4.3.2	 Anti-epileptics
		References
Part IV: Treatment of Pathologic Myopia
	29: Prevention of Myopia Progression in Children and Adolescents
		29.1	 Introduction
		29.2	 Emmetropization
		29.3	 Environmental Risk Factors for Axial Elongation
		29.4	 Outdoor Activities
		29.5	 Optical Intervention
			29.5.1	 Undercorrection
			29.5.2	 Part-Time Full Correction
			29.5.3	 Progressive Addition Lenses
			29.5.4	 Contact Lenses (CLs)
		29.6	 Orthokeratology
		29.7	 Pharmacological Interventions
			29.7.1	 Atropine Eye Drops
		29.8	 Pirenzepine 2% Gel
		29.9	 Conclusion
		References
	30: Optical Methods to Slow the Progression of Myopia
		30.1	 Introduction
		30.2	 Spectacle Correction
		30.3	 Contact Lenses
		30.4	 Outside Exposure
		30.5	 Combined Treatment
		30.6	 Clinical Guidelines
		References
	31: Sclera-Targeted Therapies for Pathologic Myopia
		31.1	 Scleral Reinforcement Surgery
		31.2	 Scleral Shortening with Scleral Resection or Scleral Folding
		31.3	 Scleral Strengthening
		31.4	 Scleral Collagen Cross-linking
		31.5	 Regenerative Therapy Targeting the Sclera
		31.6	 Closing Remarks
		References
Index