Difference between revisions of "Macular degeneration" - New World Encyclopedia

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{{DiseaseDisorder infobox |
 
{{DiseaseDisorder infobox |
 
   Name        = Macular degeneration |
 
   Name        = Macular degeneration |
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Image          = Intermediate age related macular degeneration.jpg |
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Caption        = Picture of the [[retina|back of the eye]] showing intermediate age-related macular degeneration |
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ICDO        = |
 
   ICD10      = {{ICD10|H|35|3|h|30}} |
 
   ICD10      = {{ICD10|H|35|3|h|30}} |
   ICD9        = {{ICD9|362.5}} |
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   ICD9        = {{ICD9|362.50}} |
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DiseasesDB    = 11948 |
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eMedicineSubj  = article |
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eMedicineTopic = 1223154 |
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MedlinePlus    = 001000 |
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MeshID        = D008268 |
 
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}}
  
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'''Macular degeneration''' is a [[medicine|medical]] condition in which there is deterioration in the macula area of the [[retina]], leading to a corresponding loss in central vision, which entails the ability to see fine details, to read, or to recognize faces. The macula area entails the light-sensitive cells at the center of inner lining of the [[eye]] (retina). In macular degeneration, this area of the retina may suffer thinning, atrophy, and in some cases, bleeding. This can result in loss of central vision,
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Macular degeneration is predominately found in elderly adults and is the leading cause of central vision loss ([[blindness]], although not loss of peripheral vision) in the United States today, for those over the age of fifty years, as well as an important cause of blindness worldwide in the elderly.<ref>P. T. de Jong, "Age-related macular degeneration," ''N Engl J Med.'' 355(2006)(14): 1474-1485.</ref> Other causes of decreased vision in the elderly include [[presbyopia]] (age related changes), [[cataracts]], [[glaucoma]], and diabetic retinopathy.
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The term macular degeneration generally refers to age-related macular degeneration (AMD or ARMD), while similar changes that affect younger individuals are referred to as some macular dystrophies. Examples of disease causing macular dystrophies in children include Best's disease, Doyne's honeycomb retinal dystrophy, Sorsby's disease, and Stargardt's disease.
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{{toc}}
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As with other disorders, personal responsibility is important. Two of the major risk factors associated with the disease, one's genetic predisposition ([[gene]]s and family history) and one's age, are factors that one cannot control. However, there are other risk factors that one can control: Obesity, high blood pressure, and high [[cholesterol]]. Diet can also be an aid, as [[vitamin]] supplements with high doses of antioxidants and [[zinc]] have been demonstrated to slow the progression of macular degeneration and foods rich in vitamins are a preventative measure.
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[[Image:Human eye cross-sectional view grayscale.png|right|thumb|240px|Human [[eye]] cross-sectional view. Courtesy [[National Institutes of Health|NIH]] [[National Eye Institute]]]]
  
[[Image:Human_eye_cross-sectional_view_grayscale.png|right|thumb|175px|Human [[eye]] cross-sectional view. Courtesy [[National Institutes of Health|NIH]] [[National Eye Institute]]]]
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==Macula==
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The '''macula''' or '''macula lutea''' (from [[Latin]] ''macula,'' "spot" and ''lutea,'' "yellow") is an oval [[yellow]] spot near the center of the [[retina]] of the human [[eye]]. It has a diameter of about 1.5 millimeters and is often histologically defined as having two or more layers of [[ganglion cell]]s. Near its center is the [[fovea]], a small pit that contains the largest concentration of [[cone cell]]s in the eye and is responsible for central vision.
  
[[Image:Human_eyesight_two_children_and_ball_normal_vision.jpg|right|thumb|220px|Normal vision. Courtesy [[National Institutes of Health|NIH]] [[National Eye Institute]]]]
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It is specialized for high [[Visual acuity|acuity]] vision. Within the macula are the fovea and foveola which contain a high density of [[Cone_cell|cones]] (photoreceptors with high acuity).
  
[[Image:Human_eyesight_two_children_and_ball_with_age-related_macular_degeneration.jpg|right|thumb|220px|The same view with age-related macular deneneration.]]
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==Age-related macular degeneration==
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Age-related macular degeneration (AMD) begins with characteristic yellow deposits in the macula called drusen, between the retinal pigment epithelium and the underlying choroid.  Risks of advanced stages of macular degeneration increase when the drusen are large and numerous and associated with disturbance in the pigmented cell layer under the macula. Advanced AMD, which is responsible for profound vision loss, has two forms: Dry and wet. Dry forms tend to be less severe then wet forms, but both should be taken seriously.
  
'''Macular degeneration''' is a medical condition predominantly found in elderly adults in which the center of the inner lining of the eye, known as the [[macula]] area of the [[retina]], suffers thinning, atrophy, and in some cases bleeding. This can result in loss of central vision, which entails inability to see fine details, to read, or to recognize faces. According to the [[American Academy of Ophthalmology]], it is the leading cause of central vision loss ([[blindness]]) and in the [[United States]] today for those over the age of fifty years. Although some macular dystrophies that affect younger individuals are sometimes referred to as macular degeneration, the term generally refers to age-related macular degeneration (AMD or ARMD).
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=====Dry macular degeneration=====
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Central geographic atrophy, the dry form of advanced AMD, progresses much slower then the wet form, and in many cases, the vision loss is less severe. The macula deteriorates over time where the pigmented retinal epithelial (a cell layer housed in the back of the eye) gradually diminishes.  This causes the vision loss in the central part of the [[eye]] through the photoreceptors (more commonly know as rods and cones). One with AMD may find their vision blurry as well as observing that colors appear gray.<ref>Kierstan Boyd, [http://www.aao.org/eye-health/diseases/amd-symptoms Macular Degeneration Symptoms] ''Eye Health'', American Academy of Ophthalmology. Retrieved September 22, 2016. </ref>
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Those with the dry version of macular degeneration will find it difficult to adapt to environments with dim lighting and will constantly need bright illumination, especially when doing close work. A sufferer may also notice blurriness of printed words, a decrease in the intensity of colors, and a blind spot in the center of their visual field.<ref>Mayo Foundation for Medical Education and Research, [http://www.mayoclinic.com/health/macular-degeneration/DS00284/DSECTION=4 Dry Macular Degeneration: Symptoms and causes] Retrieved September 22, 2016.</ref>
  
==Age related macular degeneration==
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While no treatment is available for this condition, vitamin supplements with high doses of antioxidants (lutein and zeaxanthin) and [[zinc]], have been demonstrated to slow the progression of dry macular degeneration, especially in patients with moderate to severe forms of the disease.<ref>W. G. Christen, R. J. Glynn, and C. H. Hennekens, "Antioxidants and age-related eye disease. Current and future perspectives," ''Ann Epidemiol'' 6(1996): 60.</ref>
Age-related macular degeneration begins with characteristic yellow deposits in the macula (central area of the retina) called [[drusen]].  Most people with these early changes have good vision.  People with drusen can go on to develop advanced AMD. The risk is considerably higher when the drusen are large and numerous and associated with disturbance in the pigmented cell layer under the macula. Recent research suggests that large and soft drusen are related to elevated cholesterol deposits and may respond to cholesterol lowering agents or the Rheo Procedure.  
 
  
Advanced AMD, which is responsible for profound vision loss, has two forms: dry and wet. Central geographic atrophy, the dry form of advanced AMD, results from atrophy to the retinal pigment epithelial layer below the retina, which causes vision loss through loss of photoreceptors (rods and cones) in the central part of the eye. While no treatment is available for this condition, vitamin supplements with high doses of antioxidants, Lutein and Zeaxanthin, have been demonstrated by the National Eye Institute and others to slow the progression of dry macular degeneration and in some patients, improve visual acuity.
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=====Wet macular degeneration=====
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In the wet form of AMD, also known as neovascular or exudative macular degeneration, abnormal blood vessels grow underneath the retina in the choriocapillaries, through Bruch's membrane, ultimately leading to blood and protein leakage below the macula. Bleeding, leaking, and scarring from these blood vessels eventually leads to irreversible damage of the photoreceptors and rapid vision loss if left untreated. Senile disciform degeneration (also known as Kuhnt-Junius macular degeneration), is a severe wet form that causes hemorrhaging of the blood vessels. The wet form progresses more rapidly than the dry form, and causes more severe damage. About 10 percent of dry forms may develop to wet forms.  
  
[[Neovascular]] or [[exudative]] AMD, the wet form of advanced AMD, causes vision loss due to abnormal blood vessel growth in the choriocapillaries, through [[Bruch's membrane]], ultimately leading to blood and protein leakage below the macula. Bleeding, leaking, and scarring from these blood vessels eventually cause irreversible damage to the photoreceptors and rapid vision loss if left untreated.
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A patient with this form of AMD, will note that straight lines will appear wavy and a central blind spot will form. In addition, he or she may see objects appearing smaller or farther away as compared to reality. As with the dry form, patients will also develop a central blurry spot.
  
Until recently, no effective treatments were known for wet macular degeneration. However, new drugs, called anti-VEGF (anti-Vascular Endothelial Growth Factor) agents, when injected directly into the vitreous humor of the eye using a small, painless needle, can cause contraction of the abnormal blood vessels and improvement of vision. The injections frequently have to be repeated on a monthly or bi-monthly basis. Examples of these agents include Lucentis, Avastin and Macugen. Only Lucentis and Macugen are FDA approved as of April 2007, and only Lucentis and Avastin appear to be able to improve vision, but the improvements are slight and do not restore full vision.
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Until recently, no effective treatments were known for wet macular degeneration. However, new drugs, called anti-angiogenics or anti-VEGF (anti-Vascular Endothelial Growth Factor) agents, when injected directly into the vitreous humor of the eye using a small, painless needle, can cause regression of the abnormal blood vessels and improvement of vision.<ref>P. van Wijngaarden, D. J. Coster, and K. A. Williams, Inhibitors of ocular neovascularization: promises and potential problems. ''JAMA'' 293(2005): 1509.</ref> The injections frequently have to be repeated on a monthly or bi-monthly basis. Examples of these agents include Lucentis and Avastin, both of which are FDA approved. Other therapies include thermal laser photocoagulation and photodynamic therapy depending on extent and location of lesion.
  
 
===Risk factors===
 
===Risk factors===
*'''Aging:''' Approximately 10% of patients 66 to 74 years of age will have findings of macular degeneration. The prevalence increases to 30% in patients 75 to 85 years of age.{{Fact|date=March 2007}}
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*'''Aging:''' According to researches at the Mayo Foundation for Medical Education and Research, macular degeneration is the leading cause of severe vision loss in people age 60 and older.  
*'''Smoking:''' The only environmental exposure clearly associated with macular degeneration is [[tobacco smoking]].<ref>http://news.bbc.co.uk/2/hi/health/4217010.stm</ref>  Exposure to cigarette smoke more than doubles the risk of macular degeneration.{{Fact|date=April 2007}}
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*'''Family history:''' If a patient’s family has a history of any form of AMD, he or she is more likely to develop this disease than those without a history.  
*'''Family history:''' The lifetime risk of developing late-stage macular degeneration is 50% for people who have a relative with macular degeneration vs. 12% for people who do not have relatives with macular degeneration, i.e. a four fold higher risk.{{Fact|date=March 2007}}
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*'''Macular degeneration gene:''' The genes for the complement system (a system in the body responsible for blood coagulation) proteins factor H (CFH) and factor B (CFB) have been determined to be strongly associated with a person's risk for developing macular degeneration. CFH is involved in inhibiting the [[inflammation|inflammatory]] response mediated through C3b (and the alternative pathway of complement) both by acting as a cofactor for cleavage of C3b to its inactive form, C3bi, and by weakening the active complex that forms between C3b and factor B. C-reactive protein and polyanionic surface markers such as glycosaminoglycans normally enhance the ability of factor H to inhibit complement. But the mutation in CFH (Tyr402His) reduces the affinity of CFH for CRP, and probably also alters the ability of factor H to recognize specific glycosaminoglycans. This change results in reduced ability of CFH to regulate complement on critical surfaces such as the specialized membrane at the back of the eye, thus leading to increased inflammatory response within the macula.<ref>Z. Yang, N. J. Camp, H. Sun, Z. Tong, D. Gibbs, D. J. Cameron, H. Chen, Y. Zhao, E. Pearson, X. Li, J. Chien, A. Dewan, J. Harmon, P. S. Bernstein, V. Shridhar, N. A. Zabriskie, J. Hoh, K. Howes, and K. Zhang, "A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration," ''Science.'' 314(2006)(5801): 992-993.</ref>
*'''Macular degeneration gene:''' The genes for the [[complement system]] proteins [[factor H]] (CFH) and factor B (CFB) have been determined to be strongly associated with a person's risk for developing macular degeneration. CFH is involved in inhibiting the inflammatory response mediated via C3b (and the [[Alternative Pathway]] of complement) both by acting as a cofactor for cleavage of C3b to its inactive form, C3bi, and by weakening the active complex that forms between C3b and factor B. C-reactive protein and polyanionic surface markers such as [[glycosaminoglycans]] normally enhance the ability of factor H to inhibit complement . But the mutation in CFH(Tyr402His) reduces the affinity of CFH for CRP and probably also alters the ability of factor H to recognise specific glycosaminoglycans. This change results in reduced ability of CFH to regulate complement on critical surfaces such as the specialised membrane at the back of the eye and leads to increased inflammatory response within the macula. In two 2006 studies at Yale Department of Epidemiology and Public Health and the Department of Ophthalmology and Visual Sciences, Moran Eye Center at the University of Utah School of Medicine, another gene that has implications for the disease, called HTRA1 (encoding a secreted serine protease), was identified.  <ref>Yang Z, Camp NJ, Sun H, Tong Z, Gibbs D, Cameron DJ, Chen H, Zhao Y, Pearson E, Li X, Chien J, Dewan A, Harmon J, Bernstein PS, Shridhar V, Zabriskie NA, Hoh J, Howes K, Zhang K. "A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration." ''Science.'' 2006 Nov 10;314(5801):992-3. PMID 17053109.</ref><ref>Dewan A, Liu M, Hartman S, Zhang SS, Liu DT, Zhao C, Tam PO, Chan WM, Lam DS, Snyder M, Barnstable C, Pang CP, Hoh J. "A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration".  Science. 2006 Nov 10;314(5801):989-92. PMID 17053108 </ref>
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*'''Hypertension and cardiovascular status:''' High blood pressure, high cholesterol, and obesity are a few other risk factors for macular degeneration.<ref>J. P. SanGiovanni, E. Y. Chew, T. E. Clemons, M. D. Davis, F. L. Ferris, G. R. Gensler, N. Kurinij, A. S. Lindblad, R. C. Milton, J. M. Seddon, and R. D. Sperduto, [http://archopht.ama-assn.org/cgi/content/short/125/5/671 The relationship of dietary lipid intake and age-related macular degeneration in a case-control study,] ''Archives of Ophthamology'' 125(2007): 671-679. Retrieved September 22, 2016.</ref>
*'''Hypertension''': Also known as [[high blood pressure]].
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*'''Oxidative stress:''' It has been proposed that age related accumulation of low molecular weight, phototoxic, pro-oxidant melanin oligomers within lysosomes in the retinal pigment epithelium may be partly responsible for decreasing the digestive rate of photoreceptor outer rod segments (POS) by the RPE. A decrease in the digestive rate of POS has been shown to be associated with lipofuscin formation&mdash;a classic sign associated with macular degeneration.<ref>R. Sarangarajan, and S. P. Apte, "Melanin aggregation and polymerization: possible implications in age related macular degeneration," ''Ophthalmic Research'' 37(2005): 136-141.</ref>
*'''Cardiovascular status''' - high cholesterol, [[obesity]].
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*'''Sex:''' Women are at a much higher risk of developing macular degeneration than men, especially since they tend to live longer.
*'''High fat intake''' is associated with an increased risk of macular degeneration in both women and men. Fat provides about 42% of the [[food energy]] in the average American diet. A diet that derives closer to 20-25% of total food energy from fat is probably healthier. Reducing fat intake to this level means cutting down greatly on consumption of red meats and dairy products such as milk, cheese, and butter. Eating more cold-water fish<ref name='areds20'> {{cite web|url=http://archopht.ama-assn.org/cgi/content/short/125/5/671 |title=The Relationship of Dietary Lipid Intake and Age-Related Macular Degeneration in a Case-Control Study |last=John Paul SanGiovanni, ScD; Emily Y. Chew, MD; Traci E. Clemons, PhD; Matthew D. Davis, MD; Frederick L. Ferris III, MD; Gary R. Gensler, MS; Natalie Kurinij, PhD; Anne S. Lindblad, PhD; Roy C. Milton, PhD; Johanna M. Seddon, MD; and Robert D. Sperduto, MD |date=May 5, 2007 |work=Archives of Ophthamology }}</ref> (at least twice weekly), rather than red meats, and eating any type of nuts may help macular degeneration patients.<ref>[http://www.agingeye.net/maculardegen/maculardegeninformation.php Macular degeneration Types and Risk Factors]</ref>
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*'''Race:''' Macular degeneration is more likely to be found in whites than in any other race.<ref>Age-Related Eye Disease Study Research Group, "Risk factors associated with age-related macular degeneration. A case-control study in the age-related eye disease study: Age-Related Eye Disease Study Report Number 3." ''Ophthalmology.'' 107(2000)(12): 2224-2232.</ref>  
*'''Oxidative stress:''' It has been proposed that age related accumulation of low molecular weight, phototoxic, [[pro-oxidant]] [[melanin]] oligomers within lysosomes in the [[retinal pigment epithelium]] may be partly responsible for decreasing the digestive rate of photoreceptor outer rod segments (POS) by the RPE. A decrease in the digestive rate of POS has been shown to be associated with [[lipofuscin]] formation - a classic sign associated with macular degeneration.<ref>"Melanin aggregation and polymerization: possible implications in age related macular degeneration." ''Ophthalmic Research'', 2005; volume 37: pages 136-141. </ref>
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*'''Exposure to sunlight (especially blue light):''' Exposure to sunlight may also contribute to the development of macular degeneration. This is because the eye’s retina is more sensitive to ultraviolet light (UV).
*'''Race''' Macular degeneration is more likely to be found in whites than in blacks.<ref>Age-Related Eye Disease Study Research Group. "Risk factors associated with age-related macular degeneration. A case-control study in the age-related eye disease study: Age-Related Eye Disease Study Report Number 3." ''Ophthalmology.'' 2000 Dec;107(12):2224-32. PMID 11097601.</ref><ref>Clemons TE, Milton RC, Klein R, Seddon JM, Ferris FL 3rd; Age-Related Eye Disease Study Research Group. "Risk factors for the incidence of Advanced Age-Related Macular Degeneration in the Age-Related Eye Disease Study (AREDS) AREDS report no. 19." ''Ophthalmology.'' 2005 Apr;112(4):533-9. PMID 15808240.</ref>
 
*'''Exposure to sunlight''' especially blue light. There is conflicting evidence as to whether exposure to sunlight contributes to the development of macular degeneration. A recent study in the ''British Journal of Ophthalmology'' on 446 subjects found that it does not.<ref>{{cite journal | first = JC | last = Khan | coauthors = Shahid H, Thurlby DA, Bradley M, Clayton DG, Moore AT, Bird AC, Yates JR, Genetic Factors in AMD Study | year = 2006 | month = Jan | title = Age related macular degeneration and sun exposure, iris colour, and skin sensitivity to sunlight | journal = The British Journal of Ophthalmology | volume = 90 | issue = 1 | pages = 29-32 | id = PMID 16361662 | accessdate = 2006-10-23}}</ref>  [[High energy visible light]] (HEV) has been implicated as a cause of age-related macular degeneration.<ref>{{cite journal | first = C | last = Glazer-Hockstein | coauthors = Dunaief JL | year = 2006 | month = Jan | title = Could blue light-blocking lenses decrease the risk of age-related macular degeneration? | journal = Retina | volume = 26 | issue = 1 | pages = 1-4 | id = PMID 16395131 | accessdate = 2006-10-23}}</ref><ref>{{cite journal | first = TH | last = Margrain | coauthors = Boulton M, Marshall J, Sliney DH | year = 2004 | month = Sep | title = Do blue light filters confer protection against age-related macular degeneration? | journal = Progress in Retinal and Eye Research | volume = 23 | issue = 5 | pages = 523-31 | id = PMID 15302349 | accessdate = 2006-10-23}}</ref>
 
  
 
===Signs===
 
===Signs===
*[[Drusen]]
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Macular degeneration destroys one's sharp, central vision. Some common signs of macular degeneration include the need for more light when looking at anything close up. Fine typeface and other details will become more difficult to read, as well as text on signs. In addition, a sufferer will see gray or blank spots in the center of their field of vision, adding to visible difficulties.
*Pigmentary alterations
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*Exudative changes: [[hemorrhages]] in the eye, hard exudates, subretinal/sub-RPE/intraretinal fluid
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=====Other signs include the following:=====
*Atrophy: incipient and geographic
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* Drusen—characterized by yellow deposits in the macula
*Visual acuity drastically decreasing (two levels or more) ex: 20/20 to 20/80.
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* Pigmentary alterations  
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* Exudative changes: Hemorrhages in the eye, hard exudates, subretinal/sub-RPE/intraretinal fluid  
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* Atrophy: Incipient and geographic  
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* Visual acuity drastically decreasing (two levels or more) ex: 20/20 to 20/80.
  
 
===Symptoms===
 
===Symptoms===
[[Image:Amsler.jpg|thumb|220px|right|Image courtesy [http://www.agingeye.net/ AgingEye Times] ]]
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[[File:Eye disease simulation, normal vision.jpg|right|250px|thumb|Normal vision]]
*Blurred vision: Those with nonexudative macular degeneration may by asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss.
 
*Central scotomas (shadows or missing areas of vision)
 
*Distorted vision (i.e. ''metamorphopsia'') - A grid of straight lines appears wavy and parts of the grid may appear blank.  Patients often first notice this when looking at mini-blinds in their home.
 
*Trouble discerning colors; specifically dark ones from dark ones and light ones from light ones.
 
*Slow recovery of visual function after exposure to bright light
 
  
The '''Amsler Grid Test''' is one of the simplest and most effective methods for patients to monitor the health of the macula. The [[Amsler Grid]] is essentially a pattern of intersecting lines (identical to graph paper) with a black dot in the middle. The central black dot is used for fixation (a place for the eye to stare at). With normal vision, all lines surrounding the black dot will look straight and evenly spaced with no missing or odd looking areas when fixating on the grid's central black dot. When there is disease affecting the macula, as in macular degeneration, the lines can look bent, distorted and/or missing.  
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[[File:Eye disease simulation, age-related macular degeneration.jpg|right|250px|thumb|The same view with age-related macular degeneration ([http://www.nei.nih.gov/photo/sims/images/amac_lg.jpg National Eye Institute)]]]
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* '''Blurred vision:''' Those with nonexudative macular degeneration may notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss.  
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* '''Central scotomas:''' There may be shadows or missing areas of vision.  
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* '''Distorted vision (such as metamorphopsia):''' A grid of straight lines appears wavy and parts of the grid may appear blank. Patients often first notice this when looking at mini-blinds in their home.
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* '''Trouble discerning colors:''' This may specifically involve trouble discerning dark ones from dark ones and light ones from light ones.  
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* '''Slow recovery of visual function after exposure to bright light'''
  
'Vision loss' or 'blindness' in macular degeneration refers to the loss of 'central vision' only. The peripheral vision is preserved. Blindness in macular degeneration does not mean 'inability to see light' and even with far advanced macular degeneration, the peripheral retina allows for useful vision.
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"Vision loss" or "blindness" in macular degeneration refers to the loss of "central vision" only. The peripheral vision is not affected. Blindness in macular degeneration does not mean "inability to see light" and even with far advanced macular degeneration, the peripheral retina allows for useful vision. The loss of central vision affects visual functioning, such as the ability to read.  In some cases, the disease only affects one eye at a time, making it more difficult to identify macular degeneration.
  
The loss of central vision profoundly affects visual functioning. It is not possible, for example, to read without central vision. Pictures which attempt to depict the central visual loss of macular degeneration with a black spot do not really do justice to the devastating nature of the visual loss. This can be demonstrated by printing letters 6 inches high on a piece of paper and attempting to identify them while looking straight ahead and holding the paper slightly to the side.  Most people find this surprisingly difficult to do.
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Similar symptoms with a very different etiology and different treatment can be caused by epiretinal membrane or macular puckeror leaking blood vessels in the eye.
  
Similar symptoms with a very different etiology and different treatment can be caused by [[Epiretinal membrane]] or [[macular pucker]]or leaking blood vessels in the eye..
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===Other forms===
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Other less common forms of macular degeneration include:
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* '''Cystoid macular degeneration.''' This is loss of vision in the macula due to fluid-filled areas (cysts) in the macular region. This may be a result of other disorders, such as aging, inflammation, or high myopia.
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* '''Diabetic macular degeneration.''' This is deterioration of the macula due to diabetes.
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* '''Juvenile macular degeneration (JMD)'''. This is a group of inherited disorders affecting children and younger adults.
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* '''Cystoid macular degeneration.''' This is the development of fluid-filled cysts (sacs) in the macular region, associated with aging, inflammation, or severe myopia.
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* '''Retinal pigment epithelial detachment.''' This is a rare form of wet MD in which fluid leakage from the choroid causes the detachment or disappearance of the pigmented retinal epithelium.
  
 
===Diagnosis===
 
===Diagnosis===
[[Fluorescein angiography]] allows for the identification and localization of abnormal vascular processes.
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Although this vision loss is irreversible, early detection may slow the progression of dry to wet AMD. Fluorescein angiography allows for the identification and localization of abnormal vascular processes. Optical coherence tomography is now used by most ophthalmologists in the diagnosis and the follow up evaluation of the response to treatment by using either Avastin or Lucentis, which are injected into the eye at various intervals.  
Optical coherence tomography is now used by most ophthalmologists in the diagnosis and the followup evaluation of the response to treatment by using either Avastin or Lucentis which are injected into the vitreous of the eye at various intervals.
 
 
 
===Treatment===
 
Most of the treatments that are available now and and currently being studied are aimed at stopping the neovascular (or wet) form of AMD.
 
 
 
In June 2006, the drug [[ranibizumab]] (Lucentis) has been approved by the FDA for use in the treatment of AMD.<ref>{{cite press release  | publisher=United States Food and Drug Administration | date=2006-06-30 | title=FDA Approves New Biologic Treatment for Wet Age-Related Macular Degeneration | url=http://www.fda.gov/bbs/topics/NEWS/2006/NEW01405.html | accessdate=2006-10-23}}</ref> Ranibizumab has been shown to halt the progression of the disease in most patients receiving the treatment.  Unlike previous treatments, a significant majority (70%) receiving ranibizumab had an improvement in vision of at least 1 letter. Up to 40% of patients had a significant vision increase of 3 lines or more.  In addition, up to 50% had a vision of 20/40 or better after 12 months of treatment.  This is significant as 20/40 is commonly seen as the vision at which a person can still drive a car.  Ranibizumab was the first therapy to show a statistically significant improvement in patient reported outcomes.<ref>{{cite journal | first = DM | last = Brown | coauthors = Kaiser PK, Michels M, Soubrane G, Heier JS, Kim RY, Sy JP, Schneider S; ANCHOR Study Group | year = 2006 | month = Oct 5 | title = Ranibizumab versus verteporfin for neovascular age-related macular degeneration | journal = New England Journal of Medicine | volume = 355 | issue = 14 | pages = 1432-44 | id = PMID 17021319 | accessdate = 2006-10-23}}</ref><ref>{{cite journal | first = PJ | last = Rosenfeld | coauthors = Brown DM, Heier JS, Boyer DS, Kaiser PK, Chung CY, Kim RY; MARINA Study Group | year = 2006 | month = Oct 5 | title = Ranibizumab for neovascular age-related macular degeneration | journal = New England Journal of Medicine | volume = 355 | issue = 14 | pages = 1419-31 | id = PMID 17021318 | accessdate = 2006-10-23}}</ref>  Ranibizumab is given as an injection into the eye. The initial studies required an injection every 4 weeks for 2 years.
 
 
 
[[Bevacizumab]] (Avastin), a drug approved for use in colon cancer, has been used by ophthalmologists in the treatment of wet macular degeneration.  Bevacizumab and ranibizumab were developed for the same monoclonal antibody parent.  However, ranibizumab has been affinity matured 140x and is a much smaller molecule than bevazicumab.  Being smaller allows ranibizumab to penetrate all layers of the retina and also to clear faster systemically from the eye.    Doubts about whether bevacizumab can penetrate the layers of the retina led to the development of ranibizumab.  There are also concerns about the safety of bevacizumab as it known to have significant systemic effects. Before Lucentis was available, bevacizumab was widely used by ophthalmologists who treat macular degeneration.  Some of their experiences with large numbers of patients with relatively short follow-up times were recently published.  No randomized controlled clinical trial with systematic safety data collection has been performed to validate its efficacy and safety with same certainty as ranibizumab.  Bevacizumab, when administered at the usual cancer treatment doses, has been shown to cause systemic adverse effects.  The most common adverse effect was hypertension.  There is a continued interest as the bevacizumab for use in the eye can be obtained for about 30-50 dollars per dose, compared to 2,000 dollars per dose for ranibizumab.  One concern is that bevacizumab is aliquotted out by compounding pharmacies from a single use vial of bevacizumab.  This may lead to degradation and impurities within the product.  Following the recommended protocol for ranibizumab costs about $50,000 per eye over two years. The National Eye Institute is planning a head-to-head ranibizumab vs. bevacizumab, randomized, controlled clinical trial for treatment of macular degeneration. Currently more than 50% of retinal specialists use bevacizumab as the first line drug (ACRS Practice Patterns Survey).
 
 
 
[[Pegaptanib]] (Macugen) was approved in 2004 for treatment of neovascular AMD.  It targets certain forms of VEGF molecules and is injected directly into the eye like ranibizumab or bevacizumab.  Although this was shown to decrease the risk of vision loss significantly compared to no treatment, it is felt to be relatively ineffective compared to the newer treatments.
 
 
 
Photodynamic therapy (PDT) with [[verteporfin]] (Visudyne) had been the treatment of choice for neovascular AMD until recently. This was the first treatment shown to decrease the chance of severe vision loss in 2 years in patients with neovascular AMD without first causing immediate vision loss at the time of the treatment. A photosenstive dye with affinity for the abnormal blood vessels are first injected through the veins.  A low-energy activating laser is then directed toward the abnormal blood vessels, causing selective damage to those blood vessels. This has also fallen out of favor as newer, more effective treatments became available.
 
 
 
Direct laser treatment for neovascular AMD was shown to decrease the chance of profound vision loss at 2 years in patients with neovascular AMD but it is seldom used as the treatment itself causes significant vision loss immediately. Infrequently, abnormal blood vessels outside of the center part of the macula are detected.  Direct laser treatment can be an effective way to treat these patients with acceptable morbidity.
 
  
Other drugs that are currently under investigation include: [[anecortave]] (Retaane), [[squalamine]] (Evizon), VEGF TRAP-EYE (made by [[Regeneron]]), and [[siRNA]]. Second generation antisense oligonucleotides [[iCo-007]] targeting the [[c-Raf|Raf-1]] kinase are also under investigation as a target for broad inhibition of multiple pro-angiogenic signals. Radiation therapy ([[brachytherapy]]) and [[rheopheresis]] are also being evaluated for wet macular degeneration.<ref>http://www.agingeye.net/maculardegen/maculardegennewdevelopments.php</ref>
+
The Amsler Grid Test is one of the simplest and most effective methods for patients to monitor the health of the macula. The Amsler Grid is essentially a pattern of intersecting lines (identical to graph paper) with a black dot in the middle. The central black dot is used for fixation (a place for the eye to stare at). With normal vision, all lines surrounding the black dot will look straight and evenly spaced with no missing or odd looking areas when fixating on the grid's central black dot. When there is disease affecting the macula, as in macular degeneration, the lines can look bent, distorted and/or missing.  
  
None of the drugs or laser treatment can restore vision to patients that have already suffered permanent damage to the photoreceptors or retinal pigmented epithelial cells due to advanced forms of AMD.  Stem cells are currently being studied as a potential solution to this problem.
+
Other forms of diagnosis include a dilated eye exam, where drops are used to dilate the pupils and the retina can be observed.
 
 
OT-551 eyedrop is currently being evaluated in an National Eye Institute-sponsored trial as a treatment for the dry form of AMD (the drug is already under investigation as a treatment for cataracts).
 
  
 
===Prevention===
 
===Prevention===
The [[Age-Related Eye Disease Study]] showed that a combination of high-dose [[beta-carotene]], [[vitamin C]], [[vitamin E]], and [[zinc]] can reduce the risk of developing advanced AMD by about 25 percent in those patients who have earlier but significant forms of the disease. This is the only proven intervention to decrease the risk of advanced AMD at this time.  A follow up study, Age-Related Eye Disease Study 2 to study the potential benefits of lutein, zeaxanthine, and fish oil, is currently underway.  
+
The Age-Related Eye Disease Study showed that a combination of high-dose beta-carotene, [[vitamin C]], vitamin E, and [[zinc]] can reduce the risk of developing advanced AMD by about 25 percent in those patients who have earlier but significant forms of the disease. This is the only proven intervention to decrease the risk of advanced AMD at this time.  
  
Anecortave acetate, (Retanne), is an anti-angiogenic drug that is given as an injection behind the eye (avoiding an injection directly into the eye) that is currently being studied as a potential way of reducing the risk of neovascular (or wet) AMD in high-risk patients.
+
Anecortave acetate, (Retanne), is an anti-angiogenic drug that is given as an injection behind the eye (avoiding an injection directly into the eye) that is currently being studied as a potential way of reducing the risk of neovascular (or wet) AMD in high-risk patients.  
  
Recent studies suggest that [[statin]]s, a family of drugs used for reducing [[cholesterol]] levels, may be effective in prevention of AMD, and in slowing its progression.<ref>http://bjo.bmjjournals.com/cgi/content/full/882/161</ref>
+
Intravitreal injection of Avastin (bevacizumab) can also improve vision and slow down the macular degeneration. Avastin is an immunoligic drug that prevents neovascularization. Hence it may also be effective in diabetic retinopathy. Avastin was initially used for the treatment of colorectal cancer.  
  
==Juvenile macular degeneration==
+
Foods containing antioxidants with vitamins A, C and E can also help prevent macular degeneration. Foods considered good sources of these nutrients also include kale, [[turnip]], greens, collard greens, romaine lettuce, [[broccoli]], zucchini, [[corn]], garden peas, and [[Brussels sprout]]s.
Juvenile macular degeneration is not a term in standard usage at this time. The preferred term for conditions that affect the macula in younger individuals related to genetics is macular dystrophy.  Examples of these include:
 
 
 
*[[Best's disease]]
 
*[[Doyne's honeycomb retinal dystrophy]]
 
*[[Sorsby's disease]]
 
*[[Stargardt's disease]]
 
  
 
==Impact==
 
==Impact==
 
Macular degeneration, in its advanced forms, can result in legal blindness, resulting in a loss of driving privileges and an inability to read all but very large type.  Perhaps the most grievous loss is the inability to see faces clearly or at all.
 
Macular degeneration, in its advanced forms, can result in legal blindness, resulting in a loss of driving privileges and an inability to read all but very large type.  Perhaps the most grievous loss is the inability to see faces clearly or at all.
  
Some of these losses can be offset by the use of adaptive devices. A closed-circuit television reader can make reading possible, and specialized screen-reading computer software, e.g., [[JAWS (screen reader)|JAWS]] for [[Microsoft Windows|Windows]], can give the blind person access to word processing, spreadsheet, financial, and e-mail access.
+
Some of these losses can be offset by the use of adaptive devices. A closed-circuit television reader can make reading possible, and specialized screen-reading computer software, for example, JAWS for Windows, can give the blind person access to word processing, spreadsheet, financial, and e-mail access.
  
==References==
+
==Notes==
{{reflist|2}}
+
<references/>
  
 
==External links==
 
==External links==
*[http://www.mdsupport.org Macular Degeneration Support]
+
All links retrieved November 5, 2022.
*[http://www.nei.nih.gov/amd/ Results from the National Eye Institute's Age Related Eye Disease Study showed that high levels of antioxidants and zinc significantly reduce the risk of advanced age-related macular degeneration (AMD) and its associated vision loss.]
+
*[https://nei.nih.gov/health/maculardegen Age-related Macular Degeneration] Resource Guide from the National Eye Institute (NEI).
*[http://www.medrounds.org/protect-your-sight/ An open-access eBook on Macular Degeneration: Protect Your Sight - How to Save your Vision in the Epidemic of Age-Related Macular Degeneration] by James C. Folk, MD and Mark E. Wilkinson, OD - Published March 2006
+
*[http://www.nei.nih.gov/amd/ Results from NEI's Age Related Eye Disease Study] showed that high levels of antioxidants and zinc significantly reduce the risk of advanced AMD and its associated vision loss.  
*[http://www.ahaf.org/macular/about/maabout.htm  Macular Degeneration Research]
+
*[http://www.medrounds.org/protect-your-sight/ An open-access eBook on Macular Degeneration: Protect Your Sight--How to Save your Vision in the Epidemic of Age-Related Macular Degeneration] by James C. Folk, MD and Mark E. Wilkinson, OD--Published March 2006.  
*[http://www.amdreport.com  Macular Degeneration 3000 word report] A Patients Guide to AMD
+
 
*[http://www.rheo.com/ Rheo.com |The RHEO procedure is a unique type of therapeutic apheresis that removes large molecules like cholesterol, fibrinogen and certain immunoglobulins from the blood.]
 
*[http://www.osnsupersite.com/ Home of Ocular Surgery News]
 
*[http://news.bbc.co.uk/2/hi/health/medical_notes/2042906.stm BBC News] &mdash; AMD from a European perspective
 
*[http://www.eyesight.org/ Macular Degeneration Foundation]
 
* {{cite web | title=Living with Macular Degeneration | url=http://healthnet.1111mb.com/2007/04/macular-degeneration-living-with.html | publisher=NLM | accessdate=2007-04-15}} video
 
*[http://www.VisionSimulations.com/ VisionSimulations.com |What the world looks like to people with various diseases and conditions of the eye]
 
*[http://www.visivite.com/vitamin-supplements-for-maculardegeneration.html Why good food isn't enough - Powerful antioxidant vitamin supplements can halt the progression of dry macular degeneration of the eye and in some people even improve vision.]
 
*[http://www.armdcook.com/ ARMD Cook |Recipes using medical guidelines for the prevention and possible reversal of MD and ARMD]
 
*[http://www.mgh.harvard.edu/wellman/ Wellman Center for Photomedicine] at [[Massachusetts General Hospital]] and [[Harvard Medical School]] information on the use of [[photomedicine]] as treatment
 
*[http://www.amdcanada.com  Age Related Macular Degeneration] amdcanada.com
 
*{{cite web |url=http://news.bbc.co.uk/2/hi/uk_news/scotland/glasgow_and_west/5168862.stm |title=Scientists seek to restore sight |accessdate=2006-07-13 |accessmonthday= |accessyear= |author= |last= |first= |authorlink= |coauthors= |date=[[2006-07-11]] |year= |month= |format= |work= |publisher=BBC News Scotland |pages= |language= |archiveurl= |archivedate=}}
 
*[http://news.bbc.co.uk/1/hi/health/6457427.stm BBC News, Friday, 16 March 2007]; Zinc could be key to eye disease
 
*[http://www.myvisiontest.com/ MyVisionTest] A free modern Amsler Grid test for macular degeneration
 
*[http://www.amdalliance.org AMD Alliance International]
 
  
 
{{Eye pathology}}
 
{{Eye pathology}}
[[Category:Life sciences]]
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[[Category:Life sciences]][[Category:Health and disease]][[Category:Diseases]]
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{{credit|Macular_degeneration|177341439|Macula|173008212}}

Latest revision as of 04:52, 5 November 2022


Macular degeneration
Intermediate age related macular degeneration.jpg

Picture of the back of the eye showing intermediate age-related macular degeneration
ICD-10 H35.3
ICD-O:
ICD-9 362.50
OMIM {{{OMIM}}}
MedlinePlus 001000
eMedicine article/1223154
DiseasesDB 11948

Macular degeneration is a medical condition in which there is deterioration in the macula area of the retina, leading to a corresponding loss in central vision, which entails the ability to see fine details, to read, or to recognize faces. The macula area entails the light-sensitive cells at the center of inner lining of the eye (retina). In macular degeneration, this area of the retina may suffer thinning, atrophy, and in some cases, bleeding. This can result in loss of central vision,

Macular degeneration is predominately found in elderly adults and is the leading cause of central vision loss (blindness, although not loss of peripheral vision) in the United States today, for those over the age of fifty years, as well as an important cause of blindness worldwide in the elderly.[1] Other causes of decreased vision in the elderly include presbyopia (age related changes), cataracts, glaucoma, and diabetic retinopathy.

The term macular degeneration generally refers to age-related macular degeneration (AMD or ARMD), while similar changes that affect younger individuals are referred to as some macular dystrophies. Examples of disease causing macular dystrophies in children include Best's disease, Doyne's honeycomb retinal dystrophy, Sorsby's disease, and Stargardt's disease.

As with other disorders, personal responsibility is important. Two of the major risk factors associated with the disease, one's genetic predisposition (genes and family history) and one's age, are factors that one cannot control. However, there are other risk factors that one can control: Obesity, high blood pressure, and high cholesterol. Diet can also be an aid, as vitamin supplements with high doses of antioxidants and zinc have been demonstrated to slow the progression of macular degeneration and foods rich in vitamins are a preventative measure.

Human eye cross-sectional view. Courtesy NIH National Eye Institute

Macula

The macula or macula lutea (from Latin macula, "spot" and lutea, "yellow") is an oval yellow spot near the center of the retina of the human eye. It has a diameter of about 1.5 millimeters and is often histologically defined as having two or more layers of ganglion cells. Near its center is the fovea, a small pit that contains the largest concentration of cone cells in the eye and is responsible for central vision.

It is specialized for high acuity vision. Within the macula are the fovea and foveola which contain a high density of cones (photoreceptors with high acuity).

Age-related macular degeneration

Age-related macular degeneration (AMD) begins with characteristic yellow deposits in the macula called drusen, between the retinal pigment epithelium and the underlying choroid. Risks of advanced stages of macular degeneration increase when the drusen are large and numerous and associated with disturbance in the pigmented cell layer under the macula. Advanced AMD, which is responsible for profound vision loss, has two forms: Dry and wet. Dry forms tend to be less severe then wet forms, but both should be taken seriously.

Dry macular degeneration

Central geographic atrophy, the dry form of advanced AMD, progresses much slower then the wet form, and in many cases, the vision loss is less severe. The macula deteriorates over time where the pigmented retinal epithelial (a cell layer housed in the back of the eye) gradually diminishes. This causes the vision loss in the central part of the eye through the photoreceptors (more commonly know as rods and cones). One with AMD may find their vision blurry as well as observing that colors appear gray.[2] Those with the dry version of macular degeneration will find it difficult to adapt to environments with dim lighting and will constantly need bright illumination, especially when doing close work. A sufferer may also notice blurriness of printed words, a decrease in the intensity of colors, and a blind spot in the center of their visual field.[3]

While no treatment is available for this condition, vitamin supplements with high doses of antioxidants (lutein and zeaxanthin) and zinc, have been demonstrated to slow the progression of dry macular degeneration, especially in patients with moderate to severe forms of the disease.[4]

Wet macular degeneration

In the wet form of AMD, also known as neovascular or exudative macular degeneration, abnormal blood vessels grow underneath the retina in the choriocapillaries, through Bruch's membrane, ultimately leading to blood and protein leakage below the macula. Bleeding, leaking, and scarring from these blood vessels eventually leads to irreversible damage of the photoreceptors and rapid vision loss if left untreated. Senile disciform degeneration (also known as Kuhnt-Junius macular degeneration), is a severe wet form that causes hemorrhaging of the blood vessels. The wet form progresses more rapidly than the dry form, and causes more severe damage. About 10 percent of dry forms may develop to wet forms.

A patient with this form of AMD, will note that straight lines will appear wavy and a central blind spot will form. In addition, he or she may see objects appearing smaller or farther away as compared to reality. As with the dry form, patients will also develop a central blurry spot.

Until recently, no effective treatments were known for wet macular degeneration. However, new drugs, called anti-angiogenics or anti-VEGF (anti-Vascular Endothelial Growth Factor) agents, when injected directly into the vitreous humor of the eye using a small, painless needle, can cause regression of the abnormal blood vessels and improvement of vision.[5] The injections frequently have to be repeated on a monthly or bi-monthly basis. Examples of these agents include Lucentis and Avastin, both of which are FDA approved. Other therapies include thermal laser photocoagulation and photodynamic therapy depending on extent and location of lesion.

Risk factors

  • Aging: According to researches at the Mayo Foundation for Medical Education and Research, macular degeneration is the leading cause of severe vision loss in people age 60 and older.
  • Family history: If a patient’s family has a history of any form of AMD, he or she is more likely to develop this disease than those without a history.
  • Macular degeneration gene: The genes for the complement system (a system in the body responsible for blood coagulation) proteins factor H (CFH) and factor B (CFB) have been determined to be strongly associated with a person's risk for developing macular degeneration. CFH is involved in inhibiting the inflammatory response mediated through C3b (and the alternative pathway of complement) both by acting as a cofactor for cleavage of C3b to its inactive form, C3bi, and by weakening the active complex that forms between C3b and factor B. C-reactive protein and polyanionic surface markers such as glycosaminoglycans normally enhance the ability of factor H to inhibit complement. But the mutation in CFH (Tyr402His) reduces the affinity of CFH for CRP, and probably also alters the ability of factor H to recognize specific glycosaminoglycans. This change results in reduced ability of CFH to regulate complement on critical surfaces such as the specialized membrane at the back of the eye, thus leading to increased inflammatory response within the macula.[6]
  • Hypertension and cardiovascular status: High blood pressure, high cholesterol, and obesity are a few other risk factors for macular degeneration.[7]
  • Oxidative stress: It has been proposed that age related accumulation of low molecular weight, phototoxic, pro-oxidant melanin oligomers within lysosomes in the retinal pigment epithelium may be partly responsible for decreasing the digestive rate of photoreceptor outer rod segments (POS) by the RPE. A decrease in the digestive rate of POS has been shown to be associated with lipofuscin formation—a classic sign associated with macular degeneration.[8]
  • Sex: Women are at a much higher risk of developing macular degeneration than men, especially since they tend to live longer.
  • Race: Macular degeneration is more likely to be found in whites than in any other race.[9]
  • Exposure to sunlight (especially blue light): Exposure to sunlight may also contribute to the development of macular degeneration. This is because the eye’s retina is more sensitive to ultraviolet light (UV).

Signs

Macular degeneration destroys one's sharp, central vision. Some common signs of macular degeneration include the need for more light when looking at anything close up. Fine typeface and other details will become more difficult to read, as well as text on signs. In addition, a sufferer will see gray or blank spots in the center of their field of vision, adding to visible difficulties.

Other signs include the following:
  • Drusen—characterized by yellow deposits in the macula
  • Pigmentary alterations
  • Exudative changes: Hemorrhages in the eye, hard exudates, subretinal/sub-RPE/intraretinal fluid
  • Atrophy: Incipient and geographic
  • Visual acuity drastically decreasing (two levels or more) ex: 20/20 to 20/80.

Symptoms

Normal vision
The same view with age-related macular degeneration (National Eye Institute)
  • Blurred vision: Those with nonexudative macular degeneration may notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss.
  • Central scotomas: There may be shadows or missing areas of vision.
  • Distorted vision (such as metamorphopsia): A grid of straight lines appears wavy and parts of the grid may appear blank. Patients often first notice this when looking at mini-blinds in their home.
  • Trouble discerning colors: This may specifically involve trouble discerning dark ones from dark ones and light ones from light ones.
  • Slow recovery of visual function after exposure to bright light

"Vision loss" or "blindness" in macular degeneration refers to the loss of "central vision" only. The peripheral vision is not affected. Blindness in macular degeneration does not mean "inability to see light" and even with far advanced macular degeneration, the peripheral retina allows for useful vision. The loss of central vision affects visual functioning, such as the ability to read. In some cases, the disease only affects one eye at a time, making it more difficult to identify macular degeneration.

Similar symptoms with a very different etiology and different treatment can be caused by epiretinal membrane or macular puckeror leaking blood vessels in the eye.

Other forms

Other less common forms of macular degeneration include:

  • Cystoid macular degeneration. This is loss of vision in the macula due to fluid-filled areas (cysts) in the macular region. This may be a result of other disorders, such as aging, inflammation, or high myopia.
  • Diabetic macular degeneration. This is deterioration of the macula due to diabetes.
  • Juvenile macular degeneration (JMD). This is a group of inherited disorders affecting children and younger adults.
  • Cystoid macular degeneration. This is the development of fluid-filled cysts (sacs) in the macular region, associated with aging, inflammation, or severe myopia.
  • Retinal pigment epithelial detachment. This is a rare form of wet MD in which fluid leakage from the choroid causes the detachment or disappearance of the pigmented retinal epithelium.

Diagnosis

Although this vision loss is irreversible, early detection may slow the progression of dry to wet AMD. Fluorescein angiography allows for the identification and localization of abnormal vascular processes. Optical coherence tomography is now used by most ophthalmologists in the diagnosis and the follow up evaluation of the response to treatment by using either Avastin or Lucentis, which are injected into the eye at various intervals.

The Amsler Grid Test is one of the simplest and most effective methods for patients to monitor the health of the macula. The Amsler Grid is essentially a pattern of intersecting lines (identical to graph paper) with a black dot in the middle. The central black dot is used for fixation (a place for the eye to stare at). With normal vision, all lines surrounding the black dot will look straight and evenly spaced with no missing or odd looking areas when fixating on the grid's central black dot. When there is disease affecting the macula, as in macular degeneration, the lines can look bent, distorted and/or missing.

Other forms of diagnosis include a dilated eye exam, where drops are used to dilate the pupils and the retina can be observed.

Prevention

The Age-Related Eye Disease Study showed that a combination of high-dose beta-carotene, vitamin C, vitamin E, and zinc can reduce the risk of developing advanced AMD by about 25 percent in those patients who have earlier but significant forms of the disease. This is the only proven intervention to decrease the risk of advanced AMD at this time.

Anecortave acetate, (Retanne), is an anti-angiogenic drug that is given as an injection behind the eye (avoiding an injection directly into the eye) that is currently being studied as a potential way of reducing the risk of neovascular (or wet) AMD in high-risk patients.

Intravitreal injection of Avastin (bevacizumab) can also improve vision and slow down the macular degeneration. Avastin is an immunoligic drug that prevents neovascularization. Hence it may also be effective in diabetic retinopathy. Avastin was initially used for the treatment of colorectal cancer.

Foods containing antioxidants with vitamins A, C and E can also help prevent macular degeneration. Foods considered good sources of these nutrients also include kale, turnip, greens, collard greens, romaine lettuce, broccoli, zucchini, corn, garden peas, and Brussels sprouts.

Impact

Macular degeneration, in its advanced forms, can result in legal blindness, resulting in a loss of driving privileges and an inability to read all but very large type. Perhaps the most grievous loss is the inability to see faces clearly or at all.

Some of these losses can be offset by the use of adaptive devices. A closed-circuit television reader can make reading possible, and specialized screen-reading computer software, for example, JAWS for Windows, can give the blind person access to word processing, spreadsheet, financial, and e-mail access.

Notes

  1. P. T. de Jong, "Age-related macular degeneration," N Engl J Med. 355(2006)(14): 1474-1485.
  2. Kierstan Boyd, Macular Degeneration Symptoms Eye Health, American Academy of Ophthalmology. Retrieved September 22, 2016.
  3. Mayo Foundation for Medical Education and Research, Dry Macular Degeneration: Symptoms and causes Retrieved September 22, 2016.
  4. W. G. Christen, R. J. Glynn, and C. H. Hennekens, "Antioxidants and age-related eye disease. Current and future perspectives," Ann Epidemiol 6(1996): 60.
  5. P. van Wijngaarden, D. J. Coster, and K. A. Williams, Inhibitors of ocular neovascularization: promises and potential problems. JAMA 293(2005): 1509.
  6. Z. Yang, N. J. Camp, H. Sun, Z. Tong, D. Gibbs, D. J. Cameron, H. Chen, Y. Zhao, E. Pearson, X. Li, J. Chien, A. Dewan, J. Harmon, P. S. Bernstein, V. Shridhar, N. A. Zabriskie, J. Hoh, K. Howes, and K. Zhang, "A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration," Science. 314(2006)(5801): 992-993.
  7. J. P. SanGiovanni, E. Y. Chew, T. E. Clemons, M. D. Davis, F. L. Ferris, G. R. Gensler, N. Kurinij, A. S. Lindblad, R. C. Milton, J. M. Seddon, and R. D. Sperduto, The relationship of dietary lipid intake and age-related macular degeneration in a case-control study, Archives of Ophthamology 125(2007): 671-679. Retrieved September 22, 2016.
  8. R. Sarangarajan, and S. P. Apte, "Melanin aggregation and polymerization: possible implications in age related macular degeneration," Ophthalmic Research 37(2005): 136-141.
  9. Age-Related Eye Disease Study Research Group, "Risk factors associated with age-related macular degeneration. A case-control study in the age-related eye disease study: Age-Related Eye Disease Study Report Number 3." Ophthalmology. 107(2000)(12): 2224-2232.

External links

All links retrieved November 5, 2022.


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