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Ординатура / Офтальмология / Учебные материалы / Age-related Macular Degeneration Springer.pdf
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186

E. Midena and E. Pilotto

 

 

Summary for the Clinician

Microperimetry provides more information about functional deterioration of the macula in eyes with early and advanced AMD than could be obtained by visual acuity.

Visual function changes in AMD are characterized by the progressive deterioration of retinal Þxation and central sensitivity. Even eyes with early AMD and normal visual acuity show retinal sensitivity changes. In geographic atrophy, microperimetry represents a useful prognostic biomarker. When CNV appears, Þxation deteriorates limiting reading ability, and ultimately a dense central scotoma with totally eccentric Þxation develops.

Longer duration of disease is a key factor associated with worse Þxation patterns and more retinal sensitivity deterioration.

A better understanding of the characteristics of visual function loss in AMD, obtained with microperimetry, may contribute to the clinical care of AMD patients. Microperimetry integrates other imaging techniques and allows: to monitor any phases of the disease; to optimize timing, patient selection, and treatment options in eyes with subfoveal CNV due to AMD; and to adequately quantify the beneÞcial or detrimental effects of any treatment.

References

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perimetry threshold. Eur J Ophthalmol 17:65Ð68

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5. Weingessel B, Sacu S, Vecsei-Marlovits PV et al (2009) Interexaminer and intraexaminer reliability of the microperimeter MP-1. Eye (Lond) 23:1052Ð1058

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and scanning laser ophthalmoscopeÐfundus perimetry. Am J Ophthalmol 139:125Ð134

7. Midena E, Vujosevic S, Cavarzeran F, Microperimetry Study Group (2010) Normal values for fundus perimetro with the microperimeter MP1. Ophthalmology 117:1571Ð1576, 1576.e1

8. Fujii GY, De Juan E Jr, Humayun MS et al (2003) Characteristics of visual loss by scanning laser opthalmoscope microperimetry in eyes with subfoveal choroidal neovascularization secondary to age-related macular degeneration. Am J Ophthalmol 136:1067Ð1078

9. Bellmann C, Feely M, Crossland MD, Kabanarou SA, Rubin GS (2004) Fixation stability using central and pericentral Þxation targets in patients with age-related macular degeneration. Ophthalmology 111:2265Ð2270

10. Scilley K, Jackson GR, Cideciyan AV et al (2002) Early agerelated maculopathy and self-reported visual difÞculty in daily life. Ophthalmology 109:1235Ð1242

11. Johnson PT, Brown MN, Pulliam BC et al (2005) Synaptic pathology, altered gene expression, and degeneration in photoreceptors impacted by drusen. Invest Ophthalmol Vis Sci 46:4788Ð4795

12. Midena E, Vujosevic S, Convento E et al (2007) Microperimetry and fundus autoßuorescence in patients with early age-related macular degeneration. Br J Ophthalmol 91:499Ð503

13. Schuman SG, Koreishi AF, Farsiu S et al (2009) Photoreceptor layer thinning over drusen in eyes with age-related macular degeneration imaged in vivo with Spectral-Domain optical coherence tomography. Ophthalmology 116:488Ð496

14. Sunness JS, Margalit E, Srikurnaran D et al (2007) The long-term natural history of geographic atrophy from agerelated macular degeneration. Ophthalmology 114:271Ð277

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Ophthalmol Vis Sci 50:3915Ð3921

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graphic atrophy associated with age-related macular degeneration. Am J Ophthalmol 140:1085Ð1093

18. Holz FG, Bellman C, Staudt S et al (2001) Fundus autoßuorescence and development of geographic atrophy in age-related macular degeneration. Invest Ophthalmol Vis Sci 42:1051Ð1056

19. Schmitz-Valckenberg S, Fleckenstein M, Scholl HP et al (2009) Fundus autoßuorescence and progression of agerelated macular degeneration. Surv Ophthalmol 54:96Ð117 20. Sholl HP, Bellman C, Dandekar SS, Bird AC et al (2004) Photopic and scotopic Þne matrix mapping of retinal areas of increased fundus autoßuorescence in patients with agerelated macular degeneration. Invest Ophthalmol Vis Sci

45:574Ð583

21.Schmitz-Valckenberg S, BŸltmann S, Dreyhaupt J et al (2004) Fundus autoßuorescence and fundus perimetry in the junctional zone of geographic atrophy in patients with agerelated macular degeneration. Invest Ophthalmol Vis Sci 45:4470Ð4476

11 Microperimetry

187

 

 

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27. Guez Je, Le Gargasson JF, Rigaudiere F et al (1993) Is there a systematic location for the pseudofovea in patients with central scotoma? Vision Res 33:1271Ð1279

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29. Doris N, Hart PM, Chakravarthy U et al (2001) Relation between macular morphology and visual function in patients with choroidal neovascularization of age related macular degeneration. Br J Ophthalmol 85:184Ð188

30. Cohen SY, Lamarque F, Saucet JC et al (2003) Filling-in phenomenon in patients with age-related macular degeneration: differences regarding uni-or bilaterality of central scotoma. Graefes Arch Clin Exp Ophthalmol 241:785Ð791

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32.Shiraga F (2007) Neovascular age-related macular degeneration: medical treatment. In: Midena E (ed) Perimetry and the fundus: an introduction to microperimetry. Slack incorporated, Thorofare, pp 7Ð12

33. Prager F, Michels S, Simader C et al (2008) Changes in retinal sensitivity in patients with neovascular age-related macular degeneration after systemic bevacizumab (Avastin) therapy. Retina 28:682Ð688

34. Bolz M, Simader C, Ritter M et al (2010) Morphological and functional analysis of the loading regimen with intravitreal ranibizumab in neovascular age-related macular degeneration. Br J Ophthalmol 94:185Ð189

35. Parravano MC, Oddone F, Tedeschi M et al (2009) Retinal functional changes measured by microperimetry in neovascular age-related macular degeneration patients treated with ranibizumab. Retina 29:329Ð334

36. Parravano MC, Oddone F, Tedeschi M et al (2010) Retinal functional changes measured by microperimetry in neovascular age-related macular degeneration patients treated with ranibizumab. Retina [e-pub ahead of print]

37.Squirrel DM, Mawer NP, Mody Ch et al (2010) Visual outcome after intravitreal ranibizumab for wet age-related macular degeneration. A comparison between best-corrected visual acuity and microperimetry. Retina 30:436Ð442

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Part IV

Prophylaxis and Therapy

Chapter 12 Nutritional Supplementation in AMD . . . . . . . . . . . . . . . . . .

191

Chapter 13 Laser Photocoagulation and Photodynamic Therapy . . . . . .

203

Chapter 14 Anti-VEGF-Therapy: Basics and Substances . . . . . . . . . . . .

225

Chapter 15

Anti-VEGF Therapy for AMD: Results and Guidelines . . . .

233

Chapter 16

Combination Therapies for the Treatment of AMD . . . . . . .

247

Chapter 17

Treatment Approaches for Dry AMD . . . . . . . . . . . . . . . . . . .

263

Chapter 18

Surgical Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

275

Nutritional Supplementation

12

in AMD

A.D. Meleth, V.R. Raiji,

N. Krishnadev, and E.Y. Chew

Core Messages

Nutrition, cigarette smoking, and plasma homocysteine may be modiÞable risk factors which provide therapeutic targets in the management of AMD.

Data regarding therapeutic interventions for primary prevention of AMD are limited and thus far inconclusive.

The preponderance of data regarding nutrients and AMD come from observational data. A limited number of randomized controlled trials are available to validate observational data regarding risk factors and potential therapeutic interventions for AMD.

The Age-Related Eye Disease Study (AREDS) demonstrated that daily oral supplementation of a combination of antioxidant vitamins and zinc has been shown to reduce progression to advanced AMD among patients who are at

intermediate to high risk of progression of disease [1].

The WomenÕs Antioxidant and Folic Acid Cardiovascular Study (WAFACS) demonstrated that daily long-term supplementation with folic acid, pyridoxine, B12, and cyanocobalamin reduced risk of advanced AMD in a population of female health care professionals with, or at risk for, cardiovascular disease.

The more efÞcacious combination of nutrients and antioxidants has not yet been determined.

Preliminary observational data suggests that omega-3 fatty acids and carotenoids, speciÞcally lutein and zeaxanthin, may play a role in prevention and treatment of AMD. Presently, there are insufÞcient data from randomized controlled clinical trials to make therapeutic recommendations.

A.D. Meleth (*) ¥ N. Krishnadev ¥ E.Y. Chew National Eye Institute, National Institutes of Health, Bethesda, MD, USA

e-mail: meletha@mail.nih.gov; krishnadevn@mail.nih.gov; echew@nei.nih.gov

V.R. Raiji

Department of Ophthalmology, George Washington University, Washington, DC, USA

e-mail: veena.raiji@gmail.com

12.1 Introduction

Age-related macular degeneration (AMD) is the leading cause of blindness among adults over the age of 65 years, of northern European descent in the developed countries. In the USA, the prevalence of AMD is expected to increase dramatically, from 1.75 million in 2000 to 2.95 million in 2020, due to the rapidly ageing population [1]. Given the large and now increasing burden of disease to families and to society, the identiÞcation of modiÞable risk factors and new avenues for preventive treatment have become increasingly important.

F.G. Holz et al. (eds.), Age-related Macular Degeneration,

191

DOI 10.1007/978-3-642-22107-1_12, © Springer-Verlag Berlin Heidelberg 2013