- •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
164 |
14 Combined Spectral-Domain Optical Coherence Tomography |
14
Fig. 14.9 VPA in MH. Persistent VPA has been shown to play a role in MH formation, possibly by providing ananchor for a centrifugal tangential traction. The detachment of posterior vitreous cortex (arrow) and persistent adhesion to the optic disc are shown
can develop. Studies [11] have shown that the membranes inducing pucker in eyes with MH are smaller in diameter and farther from the center of the macula than eyes with MP alone.
14.6.2.1 Lamellar Hole (LH)
LH is characterized by a thin, irregular fovea and avulsion of inner layers of the central macula. SD-OCT/SLO has proven useful in the diagnosis of LHs, which have characteristic configuration on the longitudinal scans (Fig. 14.10). Clinically, patients may retain relatively good visual acuity but in some instances surgery is indicated for distortions and loss of visual acuity.
LH is believed to result from an abortive process of MH formation, although this is by no means certain. Foveal cysts are believed to be the precursors of either full-thickness MH or LH. Indeed, a recent study [17] confirmed the presence of intraretinal cysts in both MH and LH. Interestingly, a higher prevalence of cysts was found in MH (100%) than LH (54.5%) and MP (17.9%). Similar to what was previously described for MP, VPA seems to play a role in the formation of cysts in LH as well. LH with VPA had cysts in 50% of cases, while LH without VPA only had cysts in only 20% of cases.
Based on all the aforementioned findings, it would appear that VPA is important in some, but not all vitreomaculopathies. Indeed, these diseases can be grouped according to the prevalence of VPA (in descending order) as: MH with cysts (87.5%), MP with cysts (80%), LH with cysts (50%), LH without cysts (20%), and MP without cysts (4.3%) (Fig. 14.11) [17]. Regarding intraretinal cysts, there appears to be a similar distribution with 100%
prevalence in MH with VPA, 80% in MP with VPA, 75% in LH with VPA, 42.9% of LH without VPA, and 4.3% of MP without VPA (Fig. 14.12) [35]. Thus, VPA appears to be an important factor in the pathophysiology of vitreomaculopathies, probably by influencing the vector of forces at the vitreo-retinal interface.
14.6.3 Age-Related Macular Degeneration (AMD)
The etiology of AMD is multifactorial. Risk factors include age, family history, ethnicity, cardiovascular diseases, hypertension, and cigarette smoking. AMD can be subdivided into two patterns: (a) atrophic, dry, or nonexudative AMD and (b) neovascular, wet, or exudative AMD. Dry AMD is by far the most common type, characterized by drusen and geographic atrophy. Wet AMD is characterized by neovascularization with edema and sometimes hemorrhage, causing severe vision loss. While it is known that neovascularization arises from the choriocapillaris through breaks in the Bruch’s membrane, the stimuli and true cause(s) for exudative AMD are not known.
Recent studies [36] employing ultrasound and OCT have shown that persistent vitreo-macular adhesion is more prevalent in exudative AMD (Fig. 14.13), whereas a higher prevalence of complete PVD was found in eyes with dry AMD. This suggests that vitreo-macular adhesion may be a risk factor for choroidal neovascularization and exudative changes in AMD, whereas PVD may be protective against exudative AMD. Subsequent studies confirmed these findings [37, 42] and determined that these phenomena are only important during active AMD and not in end stages such as geographic atrophy and disciform macular scarring. Furthermore, these studies showed that genetics
14.6 Vitreo-Maculopathies 165
Fig. 14.10 SD-OCT/SLO imaging of lamellar hole (LH). Combined spectral domain OCT/SLO imaging of LH demonstrates intraretinal cysts (a) and vitreous adhesion to the margins of the optic disc (b)
Vitreo-Papillary Adhesion (VPA)
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100 |
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90 |
88.2 |
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80 |
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(%) |
70 |
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60 |
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Prevalence |
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50 |
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40 |
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39.3 |
36.4 |
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30 |
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26.7 |
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20 |
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17.9 |
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10 |
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0 |
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MH |
Normals |
LH |
dry AMD |
MP |
Fig. 14.11 The prevalence of VPA in vitreo-maculopathies. The prevalence of VPA is highest in MH with cysts, followed by MP with cysts, LH with cysts, LH without cysts, and lowest in MP without cysts. Hence, VPA appears to play an important role in certain vitreo-maculopathies but not others
166 |
14 Combined Spectral-Domain Optical Coherence Tomography |
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100 |
Intra-Retinal Cysts |
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100 |
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90 |
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14 |
80 |
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80 |
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75 |
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70 |
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(%) |
60 |
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Prevalence |
50 |
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42.9 |
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40 |
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30 |
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20 |
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10 |
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4.3 |
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0 |
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MH with VPA |
MP with VPA |
LH with VPA |
LH without |
MP without |
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VPA |
VPA |
Fig. 14.12 The prevalence of intraretinal cysts in vitreo-maculopathies. The prevalence of intraretinal cysts is highest in MH with VPA, followed by MP with VPA, LH with VPA, LH without VPA, and MP without VPA. That the prevalence distribution of intraretinal cysts in various vitreo-maculopathies is similar to that of VPA suggests that VPA may influence the vectors of tractional force and cyst formation
Fig. 14.13 Vitreo-macular adhesion in exudative AMD. A higher prevalence of vitreo-macular adhesion was found in exudative age-related macular degeneration (AMD) when compared with dry AMD, suggesting that vitreo-macular adhesion may be a risk factor for exudative AMD. The posterior vitreous cortex is seen attached to the macula in the area of choroidal neovascularization in this SD-OCT/SLO scan
and environmental factors do not appear to influence the role of vitreous in exudative AMD.
14.6.4 Vitreo-Macular Traction Syndrome (VMTS)
VMTS is characterized by anomalous PVD with persistent vitreous adhesion to the macula, resulting in macular thickening, edema, and decreased visual acuity. VMTS is more prevalent in women than in men, and usually occurs in the sixth and seventh decade of life. Spontaneous
resolution may occur following complete PVD, but cell proliferation has been implicated as a possible mechanism that may hinder PVD [38]. VMTS is distinguished from MP in that there are no corrugations in the retina, since the traction is axial and not tangential. At times, this axial traction is so severe that it elevates the central retina (Fig. 14.14). Presenting symptoms are predominantly decreased central vision with less metamorphopsia than in patients with MP. The other distinguishing feature is that VMTS features fullthickness vitreous attachment to the macula, in contrast to MP where vitreoschisis splits the posterior vitreous cortex
