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Файл:Ординатура / Офтальмология / Учебные материалы / Age-related Macular Degeneration Springer.pdf
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- •Preface to the Second Edition
- •Contents
- •List of Abbreviations
- •1: Epidemiology of AMD
- •Core Messages
- •1.1 Introduction
- •1.3 Frequency
- •1.3.1 Prevalence
- •1.3.2 Incidence
- •1.4 Natural Course
- •1.5 Genetic Factors
- •1.5.1 The Complement Pathway Genes
- •1.5.1.1 Complement Factor H (CFH)
- •1.5.1.3 Complement Component 3 (C3)
- •1.5.1.4 Complement Factor I (CFI)
- •1.5.2 The ARMS2 (10q26) Locus
- •1.5.3.1 Apolipoprotein E (APOE)
- •1.5.4 Candidate Gene Association Studies
- •1.6 Environmental Factors
- •1.6.1 Smoking
- •1.6.2 Antioxidants
- •1.6.3 Body Mass Index (BMI)
- •1.6.4 Hypertension
- •1.6.5 Cataract Surgery
- •1.7 Interaction Between Risk Determinants
- •1.7.1 Combined Effects of CFH Y402H and Other Genetic and/or Environmental Factors
- •1.7.2 Combined Effects of 10q26 SNPs and Other Genetic and/or Environmental Factors
- •1.7.4 Combined Effects of the APOE Gene and Other Genetic and/or Environmental Factors
- •References
- •2: Genetics
- •Core Messages
- •2.1 Introduction
- •2.2 Identifying Risk Factors of a Common Disease
- •2.3 Early Findings
- •2.4.1 Functional Implications
- •2.5.1 Functional Implications
- •2.7 Prospects of Genetics in AMD Therapy and Prevention
- •Summary for the Clinician
- •References
- •Core Messages
- •3.1 Introduction
- •3.2 Cause and Consequences of Ageing
- •3.3 Clinical Changes Associated with Retinal Ageing
- •3.4 Ageing of the Neural Retina
- •3.5 Ageing of the RPE
- •3.5.1 Changes in RPE Cell Density
- •3.5.2 Subcellular Changes in the RPE
- •3.5.3 Accumulation of Lipofuscin
- •3.5.4 Melanosomes and Pigment Complexes
- •3.5.7 Antioxidant Capacity of the RPE
- •3.6 Ageing of Bruch’s Membrane
- •3.7 The Association Between Ageing and AMD
- •Summary for the Clinician
- •References
- •Core Messages
- •4.1 Introduction
- •4.2 The Complement System
- •4.3 Evidence for Involvement of the Complement System in AMD Pathogenesis
- •4.4.2 Complement Gene Variants and AMD Subtypes
- •4.4.3 Complement Gene Variants and Progression of AMD
- •4.4.5 Variations of Complement Genes and Response to Treatment: Pharmacogenetics
- •4.5 Emerging Pharmacological Intervention Targeting Complement Dysregulation
- •Conclusions
- •Summary for the Clinician
- •References
- •5: Histopathology
- •Core Messages
- •5.1 Retinal Pigment Epithelium
- •5.1.1 Structure and Function of the Retinal Pigment Epithelium
- •5.1.3 Deposits in the RPE
- •5.2 Bruch’s Membrane
- •5.2.1 Structure of Bruch’s Membrane
- •5.2.3 Deposits in Bruch’s Membrane, Drusen
- •5.3 Choroidal Neovascularization
- •5.4 Detachment of the Retinal Pigment Epithelium
- •5.5 Geographic Atrophy of the RPE
- •Summary for the Clinician
- •References
- •6: Early AMD
- •Core Messages
- •6.1 Introduction
- •6.2 Drusen
- •6.2.3 Fluorescence Angiography and Optical Coherence Tomography
- •6.3 Focal Hypopigmentation and Hyperpigmentation of the Retinal Pigment Epithelium
- •6.4 Abnormal Choroidal Perfusion
- •Summary for the Clinician
- •References
- •Core Messages
- •7.1 Introduction
- •7.2.1 Decreased Visual Acuity
- •7.2.2 Visual Distortion
- •7.2.3 Visual Field Defects
- •7.2.4 Miscellaneous Symptoms
- •7.3 Signs of Choroidal Neovascularization
- •7.3.1 Hemorrhage
- •7.3.2 Macular Edema and Subretinal Fluid
- •7.3.3 Retinal Pigment Epithelial Detachment
- •7.3.4 Miscellaneous Signs
- •7.4 Common Testing Modalities to Diagnose Choroidal Neovascularization
- •7.4.1 Fluorescein Angiography
- •7.4.2 Indocyanine Green Angiography
- •7.4.4 Optical Coherence Tomography
- •Summary for the Clinician
- •References
- •8: Geographic Atrophy
- •Core Messages
- •8.1 Introduction
- •8.3 Histology and Pathogenesis of Geographic Atrophy
- •8.5 Spectral Domain Optical Coherence Tomography in Geographic Atrophy
- •8.7 Risk Factors
- •8.7.1 Genetic Factors
- •8.7.2 Systemic Risk Factors
- •8.7.3 Ocular Risk Factors
- •8.8 Development of CNV in Eyes with GA
- •8.9 Visual Function in GA Patients
- •8.9.1 Measurement of Visual Acuity
- •8.9.2 Contrast Sensitivity
- •8.9.3 Reading Speed
- •8.9.4 Fundus Perimetry
- •8.10 Perspectives for Therapeutic Interventions
- •8.10.2 Complement Inhibition
- •8.10.3 Neuroprotection
- •8.10.4 Alleviation of Oxidative Stress
- •8.10.5 Serotonin-1A-Agonist
- •8.10.6 Perspective
- •Summary for the Clinician
- •References
- •9: Fundus Imaging of AMD
- •Core Messages
- •9.1 Introduction
- •9.2 Color Photography
- •9.3 Monochromatic Photography
- •9.5 Optical Coherence Tomography
- •9.5.2 Coherence Length
- •9.5.3 Time Domain Optical Coherence Tomography
- •9.5.4 Frequency Domain Optical Coherence Tomography
- •9.5.5 Increasing Depth of Imaging
- •9.5.6 General Optical Coherence Tomographic Imaging Characteristics of the Macular Region
- •9.6 Fundus Angiography
- •9.6.1 Fluorescein Dye Characteristics
- •9.6.2 Indocyanine Green Dye Characteristics
- •9.6.3 Cameras Used in Fluorescence Angiography
- •9.6.4 Patient Consent and Instruction
- •9.6.5 Fluorescein Injection
- •9.6.6 Fluorescein Technique
- •9.6.7 Indocyanine Green Technique
- •9.7 Fluorescein Angiographic Interpretation
- •9.7.1 Filling Sequence
- •9.7.2 The Macula
- •9.8 Deviations from Normal Angiographic Appearance
- •9.10.1 Drusen
- •9.12 Neovascular AMD
- •9.13 Retinal Pigment Epithelial Detachments
- •9.14 Retinal Vascular Contribution to the Exudative Process
- •9.15 Follow-up
- •9.15.1 Thermal Laser
- •9.15.2 Photodynamic Therapy
- •9.15.3 Anti-VEGF Therapy
- •Summary for the Clinician
- •References
- •10: Optical Coherence Tomography
- •10.1 Introduction
- •Core Messages
- •10.4 OCT in Geographic Atrophy
- •10.5 OCT in Exudative AMD
- •Summary for Clinician
- •References
- •11: Microperimetry
- •Core Messages
- •11.1 Introduction
- •11.2.1 From Manual to Automatic Microperimetry
- •11.2.2 Automatic Microperimetry
- •11.2.3 Microperimetry: The Examination
- •11.2.4 Microperimetry: Test Evaluation
- •11.2.5 Other Microperimeter
- •11.3 Microperimetry in AMD
- •11.3.1 Early AMD
- •11.3.2 Geographic Atrophy
- •11.3.3 Neovascular AMD
- •11.3.4 Neovascular AMD: Treatment
- •Summary for the Clinician
- •References
- •Core Messages
- •12.1 Introduction
- •12.2 Antioxidants and Zinc
- •12.3 Beta-Carotene
- •12.4 Macular Xanthophylls
- •12.6 Vitamin E
- •12.7 Vitamin C
- •12.8 Zinc
- •12.10 AREDS2
- •Summary for the Clinician
- •References
- •Core Messages
- •13.1 Introduction
- •13.2 Basic Principles
- •13.2.1 Clinical Background
- •13.2.2 Laser Photocoagulation
- •13.2.3 Photodynamic Therapy
- •13.3 Treatment Procedures
- •13.3.1 Laser Photocoagulation
- •13.3.2 Photodynamic Therapy
- •13.4 Study Results
- •13.4.1 Laser Photocoagulation
- •13.4.1.1 Extrafoveal CNV
- •13.4.1.2 Subfoveal CNV
- •13.4.1.3 Meta-analysis
- •13.4.2 Photodynamic Therapy
- •13.4.2.1 Predominantly Classic
- •13.4.2.2 Occult with No Classic Neovascularization
- •13.4.2.3 Minimally Classic
- •13.5 Safety and Adverse Events
- •13.5.1 Laser Photocoagulation
- •13.5.2 Photodynamic Therapy
- •13.6 Variations
- •13.6.1 Laser Photocoagulation: Different Wavelengths
- •13.6.2 Photodynamic Therapy
- •13.6.3 Combination Treatments
- •13.7 Present Guidelines
- •13.7.1 Laser Photocoagulation
- •13.7.2 Photodynamic Therapy
- •13.8 Perspectives
- •Summary for the Clinician
- •References
- •Core Messages
- •14.1 Introduction
- •14.2 Vascular Endothelial Growth Factor (VEGF)
- •14.3 Targets Within the VEGF Pathway
- •14.3.1 Sequestration of Released VEGF
- •14.3.2 Inhibition of VEGF and VEGF Receptor Synthesis by Small Interfering RNA (siRNA)
- •14.3.3 Inhibition of the Intracellular Signal Cascade
- •14.3.4 Natural VEGF Inhibitors
- •14.4 New Methods of Drug Delivery
- •14.5 Combined Strategies
- •Summary for the Clinician
- •References
- •Core Messages
- •15.1 Introduction
- •15.1.1 Anti-VEGF Therapies for NV-AMD
- •15.2.1 How Should Neovascular AMD be Diagnosed?
- •15.2.4.1 Results with Continuous Monthly Treatment
- •15.2.4.2 How Should Treatment be Started?
- •15.2.4.3 What Flexible Approaches Are Reported?
- •Fixed Quarterly Injection Studies
- •Flexible Dosing Regimens: Two Approaches
- •Flexible Dosing Regimens: ‘As Needed’ Approach
- •Flexible Dosing Regimens: ‘Treat-and-Extend’ Approach
- •Summary for the Clinician
- •References
- •Core Messages
- •16.1 Introduction
- •16.3 Current Limitation of Therapy in the Treatment of Exudative AMD
- •16.4 Rationale for Combination Therapy in the Treatment of Exudative AMD
- •16.5 Clinical Data Examining Combination Therapy for Exudative AMD
- •16.5.3 Triple Therapy for Exudative AMD
- •16.5.4 Combination Therapy with Radiation
- •Summary for the Clinician
- •References
- •Core Messages
- •17.1 Introduction
- •17.2 Current Treatment Options for Dry AMD
- •17.3 Targeting the Cause of AMD
- •17.4 Preclinical and Phase I Drugs in Development for Dry AMD
- •17.4.1 Clinical Trial Endpoints in Dry AMD
- •Trimetazidine
- •17.4.2.2 Neuroprotection
- •Ciliary Neurotrophic Factor (CNTF/NT-501)
- •AL-8309B (Tandospirone)
- •Brimonidine Tartrate Intravitreal Implant
- •17.4.2.3 Visual Cycle Modulators
- •Fenretinide
- •17.4.2.4 Other
- •17.4.3 Drugs to Prevent Injury from Oxidative Stress and Micronutrient Depletion
- •17.4.4.1 Complement Inhibition at C3
- •17.4.4.2 Complement Inhibition at C5
- •Eculizumab
- •17.4.4.3 Complement Inhibition of Factor D
- •FCFD4514S
- •Iluvien
- •Glatiramer Acetate (Copaxone)
- •17.5 Summary
- •Summary for the Clinician
- •References
- •18: Surgical Therapy
- •Core Messages
- •18.1 Maculoplasty
- •18.2 Macular Translocation
- •18.3 Single Cell Suspensions
- •18.5 Indications for Surgery
- •18.5.1 Non-responder
- •18.5.2 Pigment Epithelium Rupture
- •18.5.3 Massive Submacular Bleeding
- •18.5.5 Macula Dystrophies
- •Summary for the Clinician
- •References
- •19: Reading with AMD
- •Core Messages
- •19.1 Introduction
- •19.2 Physiological Principles
- •19.3 Reading with a Central Scotoma
- •19.3.1.2 The Reading Visual Field Related to the Fundus (Fig. 19.4b)
- •19.3.1.3 The Reading Visual Field Related to the Text (Fig. 19.4c)
- •19.3.1.4 Eccentric Fixation Related to the Globe (Fig. 19.5)
- •19.3.3 Examination of Fixation Behaviour
- •19.3.4 Motor Aspects
- •19.4 Methods to Examine Reading Ability
- •19.5 Rehabilitation Approaches to Improve Reading Ability
- •Summary for the Clinician
- •References
- •20: Low Vision Aids in AMD
- •Core Messages
- •20.2 Effects of Visual Impairment in AMD
- •20.5 Optical Magnifying Visual Aids for Distance
- •20.5.1 Aids for Watching Television
- •20.8 Electronic Reading Instruments
- •20.9 Additional Aids
- •20.10 Noteworthy Details for the Provision of Low Vision Aids
- •20.11 Basic Information on Prescription
- •Summary for the Clinician
- •References
- •Index
Reading with AMD |
19 |
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S. Trauzettel-Klosinski |
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Core Messages
›Reading is a crucial function, which is relevant for everyday life.
›The loss of reading ability in AMD means a serious reduction of quality of life.
›With appropriate adaptive strategies (eccentric fixation) and rehabilitation measures (visual aids and training), reading ability can be maintained or regained in most patients with AMD.
›Standardized methods for specific diagnostics are available.
Table 19.1 Reading ability means
•Independence
•Communication
•Participation in social life
•Mental agility
•Quality of life
patients, the need for rehabilitation will further increase during the next years [1–3].
Reading is neither spelling, nor an integrative view of a text. Reading is a complex sensory-motor-cogni- tive process, which can be impaired by various factors, especially by central visual field defects [4]. On the other hand, this process can also be improved by specific measures, utilizing the knowledge about the pathophysiology of reading.
19.1Introduction
The loss of reading ability is the main complaint of patients with AMD. Reading is of high significance for an independent life-style and the general quality of life (Table 19.1). Therefore, the main goal in rehabilitation of AMD patients is to maintain and to reconstitute reading ability. Due to the increasing number of AMD
S. Trauzettel-Klosinski
Low Vision Clinic and Research Laboratory, Centre for Ophthalmology, University of Tübingen, Tübingen, Germany
e-mail: susanne.trauzettel-klosinski@uni-tuebingen.de
19.2Physiological Principles
The retinal area used for reading comprises only a few square millimetres, but it is disproportionately over-rep- resentated in the visual cortex. The central 10° (diameter) of the visual field, which correspond to approximately 2% of the total visual field, utilise nearly 50% of the primary visual cortex [5].
Visual acuity decreases rapidly with increasing eccentricity (Fig. 19.1). A visual acuity of about 0.4 is necessary to recognize newspaper print at a distance of 25 cm. This visual acuity can be found at the margin of the fovea, for example.
During fixation, a group of letters is perceived and therefore, a reading visual field of a certain minimum
F.G. Holz et al. (eds.), Age-related Macular Degeneration, |
287 |
DOI 10.1007/978-3-642-22107-1_19, © Springer-Verlag Berlin Heidelberg 2013 |
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