توضیحاتی در مورد کتاب PATHOLOGIC MYOPIA
نام کتاب : PATHOLOGIC MYOPIA
عنوان ترجمه شده به فارسی : نزدیک بینی پاتولوژیک
سری :
ناشر : SPRINGER NATURE
سال نشر : 2021
تعداد صفحات : 455
ISBN (شابک) : 9783030743345 , 3030743349
زبان کتاب : English
فرمت کتاب : pdf
حجم کتاب : 40 مگابایت
بعد از تکمیل فرایند پرداخت لینک دانلود کتاب ارائه خواهد شد. درصورت ثبت نام و ورود به حساب کاربری خود قادر خواهید بود لیست کتاب های خریداری شده را مشاهده فرمایید.
فهرست مطالب :
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