- •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
Low Vision Aids in AMD |
20 |
|
|
K. Rohrschneider |
|
|
|
|
|
20.1 Definition of Visual Impairment |
|
Core Messages |
||
|
|
|
›Age-related macular degeneration leads to a loss of reading ability as a result of a central scotoma; however, it never results in complete blindness.
›The prescription of low vision aids is based on comprehensive measurement of visual acuity including inquiry into the needed magnification.
›Besides a huge number of optical low vision aids like magnifying glasses, spectacles and telescope systems, above all CCTVs are used for patients suffering from advanced functional impairment.
›Now also hand-held electronic low vision aids (LVAs) have become available.
›Television is important for the older visually impaired; here a shortening of the distance or a bigger television screen is often helpful.
›Complementary aids like a lectern or lighting are very important.
›Low vision rehabilitation is time consuming and requires experience. Nevertheless, in most cases the reading ability is accessible with simple LVAs and thus allows protecting independence of living.
K. Rohrschneider
Department of Ophthalmology, University of Heidelberg, Heidelberg, Germany
e-mail: kr@uni-hd.de
“Visual impairment” is the summarization of any impairment of the visual function of the eye following the best possible refractive correction by means of glasses or contact lenses. The degree of visual impairment depends on the cause and location of the eye disease. It is generally assessed by visual acuity in the distance, although consideration of other visual functions may also be important (Table 20.1) [1].
There are so many different definitions of visual impairment or even blindness in most countries that it is not possible to define a single one that can be universally adopted. The World Health Organization has provided a notation for classification of visual acuity, which is comparable to the German classification: categories 1–3 define low vision with reduction of visual acuity to less than 0.3, 0.1 and 0.05 (6/18, 6/60, 3/60), respectively (Table 20.1). Virtual blindness is present with a reduction of visual acuity to 0.05 (1/20), which is not as strong as the German legal definition of blindness with visual acuity 1/50 or less. However, a person will already be considered legally blind in countries such as the USA when his visual acuity is reduced to 20/200 in the better eye or if a visual field constriction of 10° or less in Goldmann perimetry is present. Furthermore, in Germany, patients with a visual acuity reduction to 0.3 or less are considered to be legally disabled.
Distance visual acuity is not the only criterion defining visual impairment. Other visual functions such as reading behaviour, visual field, mesopic functioning, color vision and contrast sensitivity also need to be taken into consideration and comparable gradings have to be found for them. For a successful visual rehabilitation of the elderly visually impaired, near visual acuity
F.G. Holz et al. (eds.), Age-related Macular Degeneration, |
295 |
DOI 10.1007/978-3-642-22107-1_20, © Springer-Verlag Berlin Heidelberg 2013 |
|
296 |
K. Rohrschneider |
|
|
Table 20.1 World Health Organization notation for classification of visual acuity
|
|
Visual acuity with the best |
|
|
|
possible correction |
|
Category of visual |
Maximum equal |
Minimum better |
|
impairment |
to or less than: |
than: |
|
1 |
(low vision) |
6/18 |
6/60 |
|
|
3/10 (0,3) |
1/10 (0,1) |
|
|
20/70 |
20/200 |
2 |
(severe low vision) |
6/60 |
3/60 |
|
|
1/10 (0,1) |
1/20 (0,05) |
|
|
20/200 |
20/400 |
3 |
(virtual blindness) |
3/60 |
1/60 (finger |
|
|
|
counting at 1 m) |
|
|
1/20 (0,05) |
1/50 (0,02) |
|
|
20/400 |
5/300 (20/1200) |
4 |
|
1/60 (finger |
Light perception |
|
|
counting at 1 m) |
|
|
|
1/50 (0,02) |
|
|
|
5/300 |
|
5 |
|
No light perception |
|
9 |
|
Undetermined or unspecified |
|
and reading ability in addition to visual field and photophobia caused by glare are most relevant.
20.2Effects of Visual Impairment in AMD
The functional damage in age-related macular degeneration (AMD) is characterized by a functional loss in the central visual field, so that the recognizing and reading ability are limited or lost. The peripheral visual field with its lower resolution is important for orientation purposes as well as for detection of movement. Patients with AMD will keep these functions for life. The remaining ability to detect movement enables these patients to move freely at home or in familiar surroundings, and after some special training also allows them to venture into the wider vicinty. Patients with AMD will never become completely blind.
The duration of the habituation phase varies. During this time it is of the utmost importance to counsel the patient with regard to his diagnosis, on the implications of his visual impairment, on how to regain his independence and on which visual aids are available for him. Thereafter, it is absolutely vital that the visually impaired familiarizes himself with his low vision aids, accepts the suggested aids and applies them frequently. This
process requires a lot of patient compliance, patience and a considerable amount of time. The elderly low vision patient will only accept being dependent on visual aids with a tremendous effort. This is mostly the case when medication as well as surgical approaches have failed. The acceptance of being visually impaired needs more time with increasing age. Fear of further increasing loss of vision should not be allowed to depress the patient or to stop him in his daily activities.
In addition to other therapeutic measures, the ophthalmologist plays an important role by alleviating the elderly visually impaired patient’s fear of becoming blind, enabling him to use his remaining visual function in a positive way and supporting his motivation to keep active and apply his low vision aids [2–4].
In patients suffering from AMD, visual acuity is reduced not only for far distances, but also for near sight. Objects at varying distances cannot be fixated on, and traffic lights, bus line numbers, street signs and faces cannot be recognized. The main handicap, however, is caused by the loss of reading ability. Headlines in the newspaper can be read, but not the articles below them. For most patients it is impossible to read their daily mail and TV journals, bills or bank account statements. Reduced near visual acuity also affects housekeeping, shopping and participation in certain hobbies.
Due to the demographic development an increasing number of elderly to very old visually impaired patients need to be provided with visual aids [5]. A certain degree of autonomy can be achieved by the use of optical and electronic visual aids. It is beneficial for the patient that there are a multitude of devices available to ensure that the visually impaired will be provided with the correct visual aid for each of the diverse and differing “visual tasks”. The wide choice of aids is an advantage, offering equipment for various visual tasks [3, 4, 6].
20.3Choosing the Required Magnification
Reading text has to be adapted to the reduced acuity as well as to the extent of the central scotoma. This means that fonts have to be enlarged accordingly. In most cases the required magnification can be easily assessed with the appropriate reading chart. Charts are available from different manufacturers, such as Keeler, Schweizer, Zeiss and others. At a defined distance of 25 cm, the magnification can be evaluated very easily.
