- •Foreword
- •Preface
- •Contents
- •Contributors
- •Chapter 1
- •1.1 Introduction
- •1.2 Limitations of Time-Domain OCT
- •1.4 Conclusion
- •References
- •Chapter 2
- •2.1 Background
- •2.3 Clinical Application
- •2.4 Conclusions
- •References
- •Chapter 3
- •Fluorescein Angiography
- •3.1 Principles of Fluorescein Angiography
- •3.2 Procedures for Fluorescein Angiography
- •3.4 Time Course of Fluorescein Angiography
- •3.5 Interpretation of Fluorescein Angiography
- •3.5.1 Hypofluorescent Lesions
- •3.5.2 Hyperfluorescent Lesions
- •3.6 Fluorescein Angiography Today
- •References
- •Chapter 4
- •Wide-Field Imaging and Angiography
- •4.1 Introduction
- •4.2 History of Fundus Imaging
- •4.3.1 Fluorescein Angiography with a Scanning Laser Ophthalmoscope
- •4.3.2 Advantages of Imaging with a Scanning Laser Ophthalmoscope
- •4.4 Clinical Use of Wide-Field Imaging
- •4.4.1 Wide-Field Imaging in Uveitis
- •4.4.4 Wide-Field Imaging of Choroidal Tumors
- •4.5 Future Directions for Fundus Imaging
- •4.6 Conclusion
- •References
- •Chapter 5
- •Autofluorescence Imaging
- •5.1 Introduction
- •5.2 What is Fundus Autofluorescence?
- •5.3 Identification of Early Disease Stages
- •5.4 Phenotyping
- •5.5 Disease Markers
- •5.6 Monitoring of Disease Progression
- •5.7 Disease Mapping
- •5.8 Functional Correlation
- •References
- •Chapter 6
- •Imaging the Macular Pigment
- •6.1 Macular Pigment
- •6.1.1 Characteristics and Potential Functions
- •6.1.3 Spatial Distribution
- •6.1.4 Modifying the Macular Pigment
- •6.1.5 MPOD and Age
- •6.2 Measurement Techniques
- •6.2.1 Heterochromatic Flickerphotometry
- •6.2.2 Fundus reflectance
- •6.2.3 Autofluorescence
- •6.2.4 Raman spectroscopy
- •6.2.5 How do different techniques compare
- •6.3 Imaging
- •6.3.1 Heterochromatic Flickerphotometry
- •6.3.2 Fundus Reflectance
- •6.3.3 Autofluorescence
- •6.3.4 Raman spectroscopy
- •References
- •Chapter 7
- •7.1 Introduction
- •7.2 Origin of Near-Infrared Autofluorescence
- •7.3 RPE Melanin: Role and Aging
- •7.4 Clinical Cases
- •7.4.1 Age-Related Macular Degeneration
- •7.4.2 Retinal Dystrophies
- •7.4.2.1 Stargardt’s Disease
- •7.4.2.2 Best’s Disease
- •7.4.2.3 Retinitis Pigmentosa
- •7.5 Conclusion
- •References
- •Chapter 8
- •8.1 Introduction
- •8.3.1.1 Classic Choroidal Neovascularization
- •8.3.1.2 Occult Choroidal Neovascularization
- •8.3.1.4 Mixed-Type Choroidal Neovascularization
- •8.3.1.5 Retinal Angiomatous Proliferation
- •8.3.3 Fibrovascular Scar
- •8.5 Conclusions
- •References
- •Chapter 9
- •9.1 Fundus Cameras
- •9.1.1 Standard Images
- •9.1.2 Wide-Angle Images
- •9.1.2.1 Pomerantzeff Equator Plus
- •9.1.2.2 RetCam™
- •RetCam™ Camera Description
- •RetCam™ Technique of Image Capture
- •RetCam™ Problems
- •9.1.2.3 Panoret™
- •9.1.2.4 Optos™
- •9.2.1 Retinal Tumors
- •9.2.1.1 Retinoblastoma
- •9.2.1.2 Astrocytic Hamartoma
- •9.2.1.4 Retinal Cavernous Hemangioma
- •9.2.1.5 Retinal Racemose Hemangioma
- •9.2.1.6 Vasoproliferative Tumor
- •9.2.2 Retinal Pigment Epithelium Tumors
- •9.2.3 Choroidal Tumors
- •9.2.3.1 Choroidal Nevus
- •9.2.3.2 Choroidal Melanoma
- •9.2.4 Anterior Segment Lesions
- •9.2.4.1 Iris Lesions
- •References
- •Chapter 10
- •Metabolic Mapping
- •10.1 Aspects of Metabolism
- •10.4.1 Technical Solution
- •10.5 Clinical Results
- •10.5.1 Age-Related Macular Degeneration
- •10.5.1.1 Detection of Alterations in Early AMD
- •10.5.1.2 Lifetime Images in Late AMD
- •Non-Exudative AMD and Geographic Atrophy
- •Exudative AMD
- •10.5.2.1 Arterial Branch Occlusion
- •10.5.3 Metabolic Alteration in Diabetes Mellitus
- •10.5.3.1 Detection of Fields of Reduced Metabolism
- •References
- •Chapter 11
- •11.1 Diabetic Macular Edema
- •11.2 Examinations in Diabetic Macular Edema
- •11.3 Treatment of Diabetic Macular Edema
- •References
- •Chapter 12
- •12.1.1 Incidence and Natural History
- •12.2 Investigation of Diagnostic Accuracy of OCT for Detection of DME
- •12.2.2 Diagnostic Accuracy of OCT for Detection of DME: Are Photography or Biomicroscopy a Valid Gold Standard?
- •12.2.3 Diagnostic Accuracy of OCT to Detect CSME Using Time-Domain OCTs: How to Use OCT Retinal Thickness Cut-Offs?
- •12.3 Use of OCT When Compared with Photography: Beyond Diagnostic Accuracy
- •12.4 Appendix: Reproducibility of OCT Retinal-Thickness Measurement in Patients with DME
- •12.4.1 How Reproducibility is Reported
- •12.4.3 Spectral-Domain OCTs Reproducibility
- •References
- •Chapter 13
- •13.2 Clinical Features
- •13.3 Examination
- •13.4 Natural History
- •13.5 Ultra-High Resolution OCT and Spectral OCT Findings in Macular Holes
- •13.6 Macular Hole Formation
- •13.7 Postoperative Appearance
- •13.8 Theory of Macular Hole Closure After Vitrectomy
- •13.9 Surgical Considerations
- •13.11 Clinical Features
- •13.12 Treatment
- •References
- •Chapter 14
- •14.1 Introduction
- •14.2 Vitreous Biochemistry
- •14.3 Vitreo-Retinal Interface Anatomy
- •14.4 Anomalous Posterior Vitreous Detachment (PVD)
- •14.5 Spectral-Domain OCT (SD-OCT)
- •14.6 Vitreo-Maculopathies
- •14.6.1 Macular Pucker (MP)
- •14.6.2 Macular Hole (MH)
- •14.6.2.1 Lamellar Hole (LH)
- •14.6.3 Age-Related Macular Degeneration (AMD)
- •14.6.4 Vitreo-Macular Traction Syndrome (VMTS)
- •14.7 Conclusion
- •References
- •Chapter 15
- •15.3 Imaging the Choroid
- •15.4 Age-Related Choroidal Atrophy
- •15.5 Choroid in High Myopia
- •15.8 Volume Rendering
- •15.9 Summary
- •References
- •Chapter 16
- •16.1 Introduction
- •16.2 Optical Coherence Tomography
- •16.3 Role of Optical Coherence Tomography
- •References
- •Chapter 17
- •17.1 Background and Motivation
- •17.2 Three-Dimensional Imaging of the Choroid
- •17.3 In Vivo Cellular Resolution Retinal Imaging
- •17.4 Polarization Sensitive Retinal OCT
- •17.5 Doppler (Blood Flow) Retinal OCT
- •References
- •Chapter 18
- •Toward Molecular Imaging
- •Summaries for the Clinician
- •References
- •Index
References 167
Fig. 14.14 Posterior vitreous adhesion in VMTS. Vitreomacular traction syndrome (VMTS) results from peripheral PVD with persistent (anomalous) vitreous adhesion to the macula. There is full-thickness (i.e., no vitreoschisis) posterior vitreous adhesion to the macula inducing such significant traction that the result is a tractional retinal detachment
leaving the outer layer of the vitreous cortex (partial thickness) still attached to the macula.
There is a broad, full-thickness posterior vitreous adhesion in VMTS, while a more focal adhesion is found in the vitreo-foveal traction syndrome (VFTS). In both instances, there is peripheral vitreo-retinal separation but persistent adhesion at the macula. The tractional forces are primarily antero-posterior, inducing retinal thickening with edema in the VMTS and a central cyst in the VFTS. There is most likely no role for vitreoschisis or VPA in VMTS or VFTS, although VPA has not been studied in this group of individuals.
Summary for the Clinician
■Owing to its intended transparency, vitreous has been difficult to image and thus overlooked as important in retinal disease. Recent advances in the understanding of vitreous biochemistry, structure, and aging have forged the unifying concept of anomalous PVD. Combined SD-OCT/SLO has enabled imaging of the vitreo-retinal interface and elucidated the pathogenic mechanisms of vitreomacular disorders, including vitreoschisis. This enhanced understanding will improve current surgical therapeutics and in the future replace surgery with pharmacologic vitreolysis.
14.7 Conclusion
Anomalous PVD is a unifying concept of vitreo-retinal diseases that brings together conditions that were previously considered disparate in origin. This perspective not only contributes to our understanding of the pathogenic mechanisms in vitreo-retinal disorders, but could also influence therapeutic approaches. The advent of SD-OCT/ SLO has enabled in vivo visualization of various diseases, and thus our understanding of pathophysiology is increasingly elucidated, and better treatments are being developed. One of the most exciting of these new modalities is pharmacologic vitreolysis [39–41, 43]. To date, this approach has been largely used as a surgical adjunct, but the future will see more preventative applications in high-risk individuals. For example, pharmacologic vitreolysis may be an effective way to lower the risk of exudative changes by inducing innocuous liquefaction of the gel and concurrent dehiscence at the vitreo-macular interface. Future studies using SD-OCT/SLO and other advanced imaging technologies will hopefully identify individuals at risk of other vitreo-retinopathies as candidates for prophylactic PVD with pharmacologic vitreolysis.
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