85-521: 387715 n/a ENSG00000254636 n/a P0C7Q2 n/a NM_001099667 n/a NP_001093137 n/a Age-related maculopathy susceptibility protein 2, is a mitochondrial protein that in humans is encoded by the ARMS2 gene . This protein -related article is a stub . You can help Misplaced Pages by expanding it . Age-related maculopathy Macular degeneration , also known as age-related macular degeneration ( AMD or ARMD ),
170-418: A chronic, painless buildup of pressure in the eye. In primary angle closure glaucoma, the iridocorneal angle is narrowed or completely closed obstructing the flow of aqueous humor to the trabecular meshwork for drainage. This is usually due to the forward displacement of the iris against the cornea, resulting in angle closure. This accumulation of aqueous humor causes an acute increase in pressure and damage to
255-522: A family of immune mediators was plentiful in drusen. Complement factor H (CFH) is an important inhibitor of this inflammatory cascade, and a disease-associated polymorphism in the CFH gene strongly associates with AMD. Thus an AMD pathophysiological model of chronic low grade complement activation and inflammation in the macula has been advanced. Lending credibility to this has been the discovery of disease-associated genetic polymorphisms in other elements of
340-402: A lack of aqueous misdirection. Also, the corneal appearance is not as hazy. A reduction in visual acuity can occur followed neuroretinal breakdown. Absolute glaucoma (H44.5) is the end stage of all types of glaucoma. The eye has no vision, absence of pupillary light reflex and pupillary response , and has a stony appearance. Severe pain is present in the eye. The treatment of absolute glaucoma
425-412: A medical emergency due to the risk of impending permanent vision loss, is characterized by sudden ocular pain, seeing halos around lights, red eye , very high intraocular pressure , nausea and vomiting, and suddenly decreased vision. Acute angle closure glaucoma may further present with corneal edema, engorged conjunctival vessels and a fixed and dilated pupil on examination. Opaque specks may occur in
510-457: A primary neurodegenerative process may be responsible for degeneration at the optic nerve head in glaucoma. This would be consistent with a possible mechanism of normal tension glaucoma (those with open-angle glaucoma with normal eye pressures) and is supported by evidence showing a correlation of glaucoma with Alzheimer's dementia and other causes of cognitive decline. Both experimental and clinical studies implicate that oxidative stress plays
595-528: A rapid increase in intraocular pressure. This may lead to intense eye pain , blurred vision , and nausea . Closed-angle glaucoma is an emergency requiring immediate attention. If treated early, it is possible to slow or stop the progression of glaucoma. Regular eye examinations, especially if the person is over 40 or has a family history of glaucoma, are essential for early detection. Treatment typically includes prescription of eye drops, medication , laser treatment or surgery. The goal of these treatments
680-515: A role for extracellular matrix metabolism in AMD progression. Variations in cholesterol metabolising genes such as the hepatic lipase , cholesterol ester transferase, lipoprotein lipase and the ATP-binding cassette A1 correlate with disease progression. The early stigmata of disease, drusen, are rich in cholesterol, offering face validity to the results of genome-wide association studies. In AMD there
765-642: A role in the pathogenesis of open-angle glaucoma as well as in Alzheimer's disease. Degeneration of axons of the retinal ganglion cells (the optic nerve) is a hallmark of glaucoma. The inconsistent relationship of glaucomatous optic neuropathy with increased intraocular pressure has provoked hypotheses and studies on anatomic structure, eye development, nerve compression trauma, optic nerve blood flow, excitatory neurotransmitter, trophic factor, retinal ganglion cell or axon degeneration, glial support cell, immune system, aging mechanisms of neuron loss, and severing of
850-423: A state department of rehabilitation. Glaucoma Glaucoma is a group of eye diseases that can lead to damage of the optic nerve . The optic nerve transmits visual information from the eye to the brain. Glaucoma may cause vision loss if left untreated. It has been called the "silent thief of sight" because the loss of vision usually occurs slowly over a long period of time. A major risk factor for glaucoma
935-442: A treatment for wet AMD but the evidence to support the use of modern stereotactic radiotherapy combined with anti-VEGF is currently uncertain and is awaiting the results of ongoing studies. Nucleoside reverse transcription inhibitors like they are used in anti-HIV therapy was associated with a reduced risk of developing atrophic macular degeneration. This is because Alu elements undergo L1 (protein) -mediated reverse transcription in
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#17330856192111020-464: Is a destructive procedure like cyclocryoapplication, cyclophotocoagulation, or injection of 99% alcohol. In glaucoma visual field defects result from damage to the retinal nerve fiber layer (RNFL). Field defects are seen mainly in primary open angle glaucoma. Because of the unique anatomy of the RNFL, many noticeable patterns are seen in the visual field. Most of the early glaucomatous changes are seen within
1105-406: Is a function of production of liquid aqueous humor by the ciliary processes of the eye, and its drainage through the trabecular meshwork. Aqueous humor flows from the ciliary processes into the posterior chamber , bounded posteriorly by the lens and the zonules of Zinn , and anteriorly by the iris . It then flows through the pupil of the iris into the anterior chamber , bounded posteriorly by
1190-607: Is a major risk factor for AMD. In Caucasian (white) skin, there is a specific group of polymorphic genes (with single nucleotide alterations) that encode for enzymes and transcription factors responsible for the early steps (including the first step, formation of L-DOPA from the amino acid tyrosine ) of the melanin synthesis pathway. Many of these enzymes and transcription factors are reviewed by Markiewicz and Idowu. Also, as reviewed by Sturm et al. "increasing intracellular concentrations of either tyrosine or L-DOPA both result in an increase in melanogenesis" or formation of
1275-612: Is a matter of debate whether every person with an elevated intraocular pressure should receive glaucoma therapy. As of 2018, most ophthalmologists favored treatment of those with additional risk factors. For eye pressures, a value of 28 hPa (21 mmHg) above atmospheric pressure 1,010 hPa (760 mmHg) is often used, with higher pressures leading to a greater risk. However, some may have high eye pressure for years and never develop damage. Conversely, optic nerve damage may occur with normal pressure, known as normal-tension glaucoma. In case of above-normal intraocular pressure,
1360-522: Is a medical condition which may result in blurred or no vision in the center of the visual field . Early on there are often no symptoms. Over time, however, some people experience a gradual worsening of vision that may affect one or both eyes. While it does not result in complete blindness , loss of central vision can make it hard to recognize faces, drive, read, or perform other activities of daily life. Visual hallucinations may also occur. Macular degeneration typically occurs in older people, and
1445-470: Is a progressive accumulation of characteristic yellow deposits, called drusen (buildup of extracellular proteins and lipids), in the macula (a part of the retina), between the retinal pigment epithelium and the underlying choroid . This accumulation is believed to damage the retina over time. Amyloid beta , which builds up in Alzheimer's disease brains, is one of the proteins that accumulate in AMD, which
1530-528: Is a reason why AMD is sometimes called "Alzheimer's of the eye" or "Alzheimer's of the retina". AMD can be divided into 3 stages: early, intermediate, and late, based partially on the extent (size and number) of drusen . AMD-like pathology begins with small yellow deposits (drusen) in the macula, between the retinal pigment epithelium and the underlying choroid. Most people with these early changes (referred to as age-related maculopathy) still have good vision. People with drusen may or may not develop AMD. In fact,
1615-488: Is also associated with genetic mutations (including OPA1 and OPTN genes). Additionally, there are some rare genetic conditions that increase the risk of glaucoma, such as Axenfeld-Rieger syndrome and primary congenital glaucoma , which is associated with mutations in CYP1B1 or LTBP2 . They are inherited in an autosomal recessive fashion. Axenfeld-Rieger syndrome is inherited in an autosomal dominant fashion and
1700-503: Is also considered as consequence and cause of vision loss which means that stress management training, autogenic training and other techniques to cope with stress can be helpful. There are several pressure-lowering medication groups that could be used in lowering the IOP, usually eyedrops. The choice of medication usually depends on the dose, duration and the side effects of each medication. However, in general, prostaglandin analogues are
1785-731: Is associated with PITX2 or FOXC1 . The total prevalence of glaucoma is about the same in North America and Asia. However, the prevalence of angle-closure glaucoma is four times higher in Asia than in North America. In the United States, glaucoma is more common in African Americans , Latinos and Asian-Americans . Other factors can cause glaucoma, known as "secondary glaucoma", including prolonged use of steroids (steroid-induced glaucoma); conditions that severely restrict blood flow to
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#17330856192111870-403: Is caused by damage to the macula of the retina . Genetic factors and smoking may play a role. The condition is diagnosed through a complete eye exam . Severity is divided into early, intermediate, and late types. The late type is additionally divided into "dry" and "wet" forms, with the dry form making up 90% of cases. The difference between the two forms is categorized by the change in
1955-601: Is increased about two- to four-fold for people who have a sibling with glaucoma. Glaucoma, particularly primary open-angle glaucoma, is associated with mutations in several genes , including MYOC , ASB10, WDR36 , NTF4 , TBK1 , and RPGRIP1 . Many of these genes are involved in critical cellular processes that are implicated in the development and progression of glaucoma, including regulation of intraocular pressure, retinal ganglion cell health, and optic nerve function. Normal-tension glaucoma, which comprises 30-90% of primary open-angle glaucoma (depending on ethnic group),
2040-509: Is increased pressure within the eye, known as intraocular pressure (IOP) . It is associated with old age, a family history of glaucoma, and certain medical conditions or the use of some medications. The word glaucoma comes from the Ancient Greek word γλαυκός ( glaukós ), meaning 'gleaming, blue-green, gray'. There are different types of glaucoma, but the most common are called open-angle glaucoma and closed-angle glaucoma . Inside
2125-603: Is intricately linked to gene-environment interactions. Key risk factors are age, race/ethnicity, smoking, and family history . Advanced age is the strongest predictor of AMD, particularly over 50. As illustrated by the Figure in this section, derived from data presented by the National Eye Institute of the United States, among those over 80 years of age, White individuals are more than 6-fold more likely to develop AMD than Black or Hispanic individuals. Thus, white background
2210-672: Is managed with vascular endothelial growth factor ( VEGF ) inhibitors. Daily use of an Amsler grid or other home visual monitoring tools can be used to monitor for development of distorted vision, which may be a sign of disease progression. Dietary supplements may be suggested for people with AMD, with the goal of reducing damage to the cells in the retina with antioxidants. The formulations commonly suggested are known as AREDS . The specific vitamins and minerals in AREDS-1 are vitamin C (500 mg), zinc (80 mg), vitamin E (400 IU), copper (2 mg) and beta-carotene (15 mg). In
2295-431: Is open-angle glaucoma with an unexplained significant rise of intraocular pressure following unknown pathogenesis. Intraocular pressure can sometimes reach 80 mmHg (11 kPa). It characteristically manifests as ciliary body inflammation and massive trabecular edema that sometimes extends to Schlemm's canal. This condition is differentiated from malignant glaucoma by the presence of a deep and clear anterior chamber and
2380-472: Is to decrease eye pressure. Glaucoma is a leading cause of blindness in African Americans , Hispanic Americans , and Asians. It occurs more commonly among older people, and closed-angle glaucoma is more common in women. In 2013 for the population aged 40-80 years the global prevalence of glaucoma was estimated at 3.54%, thus affecting 64.3 million worldwide. The same year, there were 2.97 million people in North America with open angle glaucoma. By 2040,
2465-829: Is usually asymptomatic. Intermediate AMD is diagnosed by large drusen and/or any retinal pigment abnormalities. Intermediate AMD may cause some vision loss, but, like early AMD, it is usually asymptomatic. Recently, subgroups of intermediate AMD have been identified, which have a very high risk of progression toward late AMD. This subgroup (depending on the precise definitions) is termed nascent GA and/or iRORA (incomplete retinal pigment epithelium and outer retinal atrophy). These 'high-risk' subgroups of intermediate AMD can be used to inform patients of theirs prognosis. In addition, these can be applied in clinical trials as endpoints. In late AMD, enough retinal damage occurs that, in addition to drusen, people will also begin to experience symptomatic central vision loss. The damage can either be
2550-441: The choroid outside of the fovea who don't respond to drug treatment. There is strong evidence that laser coagulation will result in the disappearance of drusen but does not affect choroidal neovascularisation . A 2007 Cochrane review on found that laser photocoagulation of new blood vessels in the choroid outside of the fovea is effective and economical method, but that the benefits are limited for vessels next to or below
2635-543: The drusen in dry AMD, see below. Early-stage and intermediate-stage AMD is managed by modifying known risk factors such as smoking cessation, management of hypertension and atherosclerosis and making dietary modifications. For intermediate-stage AMD, management also includes antioxidant and mineral supplementation. Advanced-stage AMD is managed based on the presence of choroidal neovascularization (CNV): dry AMD (no CNV present) or wet AMD (CNV present). No effective treatments exist for dry AMD. The CNV present in wet AMD
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2720-585: The lamina cribrosa . Thus increases in intraocular pressure would cause nerve damage as seen in glaucoma. The vascular theory hypothesizes that a decreased blood supply to the retinal ganglions cells leads to nerve damage. This decrease in blood supply may be due to increasing intraocular pressures, and may also be due to systemic hypotension, vasospasm or atherosclerosis. This is supported by evidence that those with low blood pressure, particularly low diastolic blood pressure, are at an increased risk of glaucoma. The primary neurodegeneration theory hypothesizes that
2805-421: The retina or ciliary body . Individuals with poor blood flow to the eye are highly at risk for this condition. Neovascular glaucoma results when new, abnormal vessels begin developing in the angle of the eye that begin blocking the drainage. People with such condition begin to rapidly lose their eyesight. Sometimes, the disease appears very rapidly, especially after cataract surgery procedures. Toxic glaucoma
2890-514: The "wet" form of advanced AMD, causes vision loss due to abnormal blood vessel growth ( choroidal neovascularization ) in the choriocapillaris , through Bruch's membrane . It is usually, but not always, preceded by the dry form of AMD. The proliferation of abnormal blood vessels in the retina is stimulated by vascular endothelial growth factor (VEGF). Because these blood vessels are abnormal, these are also more fragile than typical blood vessels, which ultimately leads to blood and protein leakage below
2975-460: The AREDS-2 formulation, lutein (10 mg) and zeaxanthin (2 mg) replaced beta-carotene due to the risk of lung cancer in smokers taking beta-carotene. There is some evidence to indicate that people with bilateral early or intermediate AMD, or intermediate AMD in one eye and advanced AMD in the other eye may benefit from vitamin and mineral supplementation. AREDS supplementation may help slow
3060-641: The American Academy of Ophthalmology. There is a glaucoma screening program in the UK. Those at risk are advised to have an eye examination at least once a year. The goal of glaucoma management for patients with increased intraocular pressure is to decrease the intraocular pressure (IOP), thus slowing the progression of glaucoma and preserving the quality of life for patients, with minimal side-effects. This requires appropriate diagnostic techniques and follow-up examinations, and judicious selection of treatments for
3145-498: The U.S. had glaucoma, with 1.49 million experiencing vision impairment due to the condition, according to a meta-analysis. The study found that Black adults were about twice as likely to be affected by glaucoma as white adults. Glaucoma prevalence was 1.62% among individuals aged 18 and older and 2.56% among those aged 40 and older, while vision-affecting glaucoma occurred in 0.57% and 0.91% of these age groups, respectively. Open angle glaucoma usually presents with no symptoms early in
3230-587: The age of fifty and in the United States is the most common cause of vision loss in this age group. About 0.4% of people between 50 and 60 have the disease, while it occurs in 0.7% of people 60 to 70, 2.3% of those 70 to 80, and nearly 12% of people over 80 years old. Early or intermediate AMD may be asymptomatic, or it may present with blurred or decreased vision in one or both eyes. This may manifest initially as difficulty with reading or driving (especially in poorly lit areas). Other symptoms of AMD include distortion of vision and blind spots (especially in and around
3315-439: The aqueous humor from the eye. This contact between iris and trabecular meshwork (TM) may gradually damage the function of the meshwork until it fails to keep pace with aqueous production, and the pressure rises. In over half of all cases, prolonged contact between iris and TM causes the formation of synechiae (effectively "scars"). These cause permanent obstruction of aqueous outflow. In some cases, pressure may rapidly build up in
3400-467: The black pigment melanin. Thus there appears to be an association between reduced L-DOPA production and white skin. As suggested by the Figure and information in this section, reduced L-DOPA, resulting in white skin, appears to be associated with an increased risk of macular degeneration for white individuals over the age of 80. AMD is a highly heritable condition. Recurrence ratios for siblings of an affected individual are three- to six-fold higher than in
3485-508: The central visual field). Other signs and symptoms of macular degeneration include: Macular degeneration by itself will not lead to total blindness. For that matter, only a small number of people with visual impairment are totally blind. In almost all cases, some vision remains, mainly peripheral. Other complicating conditions may lead to such an acute condition (severe stroke or trauma, untreated glaucoma , etc.), but few macular degeneration patients experience total visual loss. The area of
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3570-505: The central visual field, mainly in Bjerrum's area, 10-20° from fixation. Following are the common glaucomatous field defects: The United States Preventive Services Task Force stated, as of 2013, that there was insufficient evidence to recommend for or against screening for glaucoma. Therefore, there is no national screening program in the US. Screening, however, is recommended starting at age 40 by
3655-618: The complement cascade including complement component 3 (C3). A powerful predictor of AMD is found on chromosome 10q26 at LOC 387715. An insertion/deletion polymorphism at this site reduces expression of the ARMS2 gene though destabilization of its mRNA through deletion of the polyadenylation signal. ARMS2 protein may localize to the mitochondria and participate in energy metabolism, though much remains to be discovered about its function. Other gene markers of progression risk includes tissue inhibitor of metalloproteinase 3 ( TIMP3 ), suggesting
3740-486: The condition prevents the use of these tests in routine practice. Nevertheless, they can be useful in selecting patients for clinical trials and analysing their response to treatment. The three loci where identified gene variants are found are designated: The pathogenesis of age-related macular degeneration is not well known, although some theories have been put forward, including oxidative stress, mitochondrial dysfunction, and inflammatory processes. The imbalance between
3825-491: The course of the disease. However, it may gradually progress to involve difficulties with vision. It usually involves deficits in the peripheral vision followed by central vision loss as the disease progresses, but less commonly it may present as central vision loss or patchy areas of vision loss. On an eye examination, optic nerve changes are seen indicating damage to the optic nerve head (increased cup-to-disc ratio on fundoscopic examination ). Acute angle closure glaucoma,
3910-464: The cytoplasm resulting in DNA synthesis. First clinical trials are being prepared as of January 2021. Because peripheral vision is not affected, persons with macular degeneration can learn to use their remaining vision to partially compensate. Assistance and resources are available in many countries and every state in the U.S. Classes for "independent living" are given and some technology can be obtained from
3995-408: The death of photoreceptors and central vision loss. In the dry ( nonexudative ) form, drusen accumulates between the retina and the choroid , causing atrophy and scarring to the retina. In the wet (exudative) form, which is more severe, blood vessels grow up from the choroid (neovascularization) behind the retina which can leak exudate and fluid and also cause hemorrhaging. Early work demonstrated
4080-506: The development of atrophy or the onset of neovascular disease. Late AMD is further divided into two subtypes based on the types of damage: Geographic atrophy and Wet AMD (also called Neovascular AMD). Dry AMD (also called nonexudative AMD) is a broad designation, encompassing all forms of AMD that are not neovascular (wet AMD). This includes early and intermediate forms of AMD, as well as the advanced form of dry AMD known as geographic atrophy. Dry AMD patients tend to have minimal symptoms in
4165-436: The development of dry AMD and Stargardt's disease. The clinical development of this mechanism, which has the potential to clear Bruch's membrane and to reduce formation of Drusen, is in preparation. Ranibizumab , aflibercept , brolucizumab , and faricimab are approved VEGF inhibitors for the treatment of CNV in wet AMD. All three drugs are administered via intravitreal injection , meaning they are injected directly into
4250-431: The drainage angle ( gonioscopy ), and retinal nerve fiber layer assessment with a fundus examination, measuring corneal thickness ( pachymetry ), and visual field testing . Glaucoma has been classified into specific types: Primary glaucoma (H40.1-H40.2) Variants of primary glaucoma Primary angle closure glaucoma is caused by contact between the iris and trabecular meshwork, which in turn obstructs outflow of
4335-444: The earlier stages; visual function loss occurs more often if the condition advances to geographic atrophy. Dry AMD accounts for 80–90% of cases and tends to progress slowly. In 10–20% of people, dry AMD progresses to the wet type. Geographic atrophy (also called atrophic AMD) is an advanced form of AMD in which progressive and irreversible loss of retinal cells leads to a loss of visual function. There are multiple layers that make up
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#17330856192114420-404: The effectiveness of lutein and zeaxanthin as a replacement in the AREDS-2 formulation. Pegcetacoplan (Syfovre) and avacincaptad pegol (Izervay) are approved for medical use in the United States. In 2023 it was reported that the aging pigment lipofuscin can be broken down with the help of melanin and drugs through a newly discovered mechanism. The pigment lipofuscin plays a central role in
4505-407: The eye) is an important risk factor for glaucoma, but only about 10-70% of people - depending on ethnic group - with primary open-angle glaucoma actually have elevated ocular pressure. Ocular hypertension—an intraocular pressure above the traditional threshold of 21 mmHg (28 hPa) or even above 24 mmHg (32 hPa)—is not necessarily a pathological condition, but it increases
4590-423: The eye, a liquid called aqueous humor helps to maintain shape and provides nutrients. The aqueous humor normally drains through the trabecular meshwork . In open-angle glaucoma, the draining is impeded, causing the liquid to accumulate and pressure inside the eye to increase. This elevated pressure can damage the optic nerve. In closed-angle glaucoma, the drainage of the eye becomes suddenly blocked, leading to
4675-408: The eye, causing pain and redness (symptomatic, or so-called "acute" angle closure). In this situation, the vision may become blurred, and halos may be seen around bright lights. Accompanying symptoms may include a headache and vomiting. Diagnosis is made from physical signs and symptoms: pupils mid-dilated and unresponsive to light, cornea edematous (cloudy), reduced vision, redness, and pain. However,
4760-553: The eye, such as severe diabetic retinopathy and central retinal vein occlusion (neovascular glaucoma); ocular trauma (angle-recession glaucoma); plateau iris ; and inflammation of the middle layer of the pigmented vascular eye structure ( uveitis ), known as uveitic glaucoma . The main effect of glaucoma is damage to the optic nerve. Eventually, this damage leads to vision loss, which can deteriorate with time. The underlying cause of open-angle glaucoma remains unclear. Several theories exist on its exact etiology. Intraocular pressure
4845-438: The eye. Bevacizumab is another VEGF inhibitor that has been shown to have similar efficacy and safety as the previous two drugs, however, is not currently indicated for AMD. AMD can also be treated with laser coagulation therapy. A randomized control trial found that bevacizumab and ranibizumab had similar efficacy, and reported no significant increase in adverse events with bevacizumab. A 2014 Cochrane review found that
4930-442: The following clinical examinations as well as procedures and tests: Diagnosis of wet (or late stage) AMD may include the following in addition to the above tests: Treatment of AMD varies depending on the category of the disease at the time of diagnosis. In general, treatment is aimed at slowing down the progression of AMD. As of 2018, there are no treatments to reverse the effects of AMD. As of 2024, there are two drugs to dissolve
5015-681: The fovea. Photodynamic therapy has also been used to treat wet AMD. The drug verteporfin is administered intravenously; light of a certain wavelength is then applied to the abnormal blood vessels. This activates the verteporfin destroying the vessels. Cataract surgery could improve visual outcomes for people with AMD, though there have been concerns about surgery increasing the progression of AMD. A randomized controlled trial found that people who underwent immediate cataract surgery (within two weeks) had improved visual acuity and better quality of life outcomes than those who underwent delayed cataract surgery (6 months). Radiotherapy has been proposed as
5100-506: The general population. Genetic linkage analysis has identified 5 sets of gene variants at three locations on different chromosomes (1, 6 and 10) as explaining at least 50% of the risk. These genes have roles regulating the immune response, inflammatory processes and homeostasis of the retina. Variants of these genes give rise to different kinds of dysfunction in these processes. Over time, this results in accumulation of intracellular and extracellular metabolic debris. This can cause scarring of
5185-510: The individual patient. Although increased IOP is only one of the major risk factors for glaucoma, lowering it via various pharmaceuticals and/or surgical techniques is currently the mainstay of glaucoma treatment. Vascular flow and neurodegenerative theories of glaucomatous optic neuropathy have prompted studies on various neuroprotective therapeutic strategies, including nutritional compounds, some of which may be regarded by clinicians as safe for use now, while others are on trial. Mental stress
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#17330856192115270-479: The iris and anteriorly by the cornea . From here, the trabecular meshwork drains aqueous humor via the scleral venous sinus ( Schlemm's canal ) into scleral plexuses and general blood circulation. In open/wide-angle glaucoma, flow is reduced through the trabecular meshwork, due to the degeneration and obstruction of the trabecular meshwork, whose original function is to absorb the aqueous humor. Loss of aqueous humor absorption leads to increased resistance and thus
5355-415: The lens in glaucoma, known as glaukomflecken. The word is German, meaning "glaucoma-specks". Glaucoma can affect anyone. Some people have a higher risk or susceptibility to develop glaucoma due to certain risk factors . Risk factors for glaucoma include increasing age, high intraocular pressure, a family history of glaucoma, and use of steroid medication. Ocular hypertension (increased pressure within
5440-599: The macula constitutes only about 2.1% of the retina, and the remaining 97.9% (the peripheral field) remains unaffected by the disease. Even though the macula provides such a small fraction of the visual field, almost half of the visual cortex is devoted to processing macular information. In addition, people with dry macular degeneration often do not experience any symptoms but can experience gradual onset of blurry vision in one or both eyes. People with wet macular degeneration may experience acute onset of visual symptoms. The pathogenesis of age-related macular degeneration (AMD)
5525-425: The macula. Bleeding, leaking, and scarring from these blood vessels eventually cause irreversible damage to the photoreceptors and rapid vision loss if left untreated. Diagnosis of age-related macular degeneration depends on signs in the macula , not necessarily vision. Early diagnosis of AMD can prevent further visual deterioration and potentially improve vision. Diagnosis of dry (or early stage) AMD may include
5610-419: The macula. Those with dry form AMD have drusen , cellular debris in their macula that gradually damages light-sensitive cells and leads to vision loss. In wet form AMD, blood vessels grow under the macula, causing blood and fluid to leak into the retina. Exercising, eating well, and not smoking may reduce the risk of macular degeneration. There is no cure or treatment that restores the vision already lost. In
5695-524: The majority of cases are asymptomatic. Prior to the very severe loss of vision, these cases can only be identified by examination, generally by an eye care professional. Developmental glaucoma (Q15.0) Secondary glaucoma (H40.3-H40.6) Neovascular glaucoma , an uncommon type of glaucoma, is difficult or nearly impossible to treat, and is often caused by proliferative diabetic retinopathy (PDR) or central retinal vein occlusion (CRVO). It may also be triggered by other conditions that result in ischemia of
5780-443: The majority of people over age 60 have drusen with no adverse effects. The risk of developing symptoms is higher when the drusen are large and numerous, and associated with the disturbance in the pigmented cell layer under the macula. Large and soft drusen are thought to be related to elevated cholesterol deposits. Early AMD is diagnosed based on the presence of medium-sized drusen, about the width of an average human hair. Early AMD
5865-431: The mechanism of open-angle glaucoma is believed to be the impeded exit of aqueous humor through the trabecular meshwork, while in closed-angle glaucoma the iris blocks the trabecular meshwork. Diagnosis is achieved by performing an eye examination . Often, the optic nerve shows an abnormal amount of cupping . Positive family history is a risk factor for glaucoma. The relative risk of having primary open-angle glaucoma
5950-444: The medical community is still not certain. Recent studies have begun to look at each layer individually. They found that decreased blood flow in the choriocapillaris precedes atrophy of the retinal pigment epithelium and the overlying photoreceptors. Since the choriocapillaris is a vascular layer, this may be used as an argument for why geographic atrophy could be a disease due to decreased blood flow. Neovascular or exudative AMD,
6035-467: The nerve fibers at the scleral edge. Screening for glaucoma is an integral part of a standard eye examination performed by optometrists and ophthalmologists. The workup for glaucoma involves taking a thorough case history, with the emphasis on assessment of risk factors. The baseline glaucoma evaluation tests include intraocular pressure measurement by using tonometry, anterior chamber angle assessment by optical coherence tomography , inspecting
6120-438: The optic nerve. The pathophysiology of glaucoma is not well understood. There are several theories regarding the mechanism of the damage to the optic nerve in glaucoma. The biomechanical theory hypothesizes that the retinal ganglion cell axons (which form the optic nerve head and the retinal nerve fiber layer) are particularly susceptible to mechanical damage from increases in the intraocular pressure as they pass through pores at
6205-448: The outside world, into an electrical signal to be sent to the brain. There are several functions of the retinal pigment epithelium. One of the main functions of the retinal pigment epithelium is to minimize oxidative stress. It does so by absorbing light, and thus preventing it from getting to the underlying layers. The layers underlying the retinal pigment epithelium are very vascularlized so they have very high oxygen tension. Thus, if light
6290-416: The patients always receive treatment, but the interval to the next visit is extended if the lesion was inactive. Recently, researchers have started to apply AI algorithms to predict the future need for treatment. The American Academy of Ophthalmology practice guidelines do not recommend laser coagulation therapy for macular degeneration, but state that it may be useful in people with new blood vessels in
6375-756: The prevalence of all types of glaucoma was projected to increase to 111.82 million worldwide and to 4.72 million in North America. Globally, glaucoma is the second-leading cause of blindness , while cataracts are a more common cause. In the United States, glaucoma is a leading cause of blindness for African Americans, who have higher rates of primary open-angle glaucoma, and Hispanic Americans . Bilateral vision loss can negatively affect mobility and interfere with driving. A meta-analysis published in 2009 found that people with primary open angle glaucoma do not have increased mortality rates , or increased risk of cardiovascular death. A 2024 JAMA Ophthalmology reports that in 2022 an estimated 4.22 million people in
6460-522: The production of damaged cellular components and degradation leads to the accumulation of harmful products, for example, intracellular lipofuscin and extracellular drusen. Incipient atrophy is demarcated by areas of retinal pigment epithelium (RPE) thinning or depigmentation that precede geographic atrophy in the early stages of AMD. In advanced stages of AMD, atrophy of the RPE (geographic atrophy) and/or development of new blood vessels (neovascularization) result in
6545-412: The progression to more severe forms of AMD and there is some evidence of improved visual acuity at 5 years. There is no evidence that micronutrient supplementation prevents AMD progression in those with severe disease or prevents disease onset in those without AMD. With regards to AREDS-1 compared with AREDS-2 formulations, there is only weak evidence comparing the effectiveness of each formulation and
6630-406: The retina or breakdown of its vascularization. The list of genetic variations association with AMD include complement factors , apolipoprotein E , fibroblast growth factor 2 , DNA excision repair protein, and age-related maculopathy susceptibility protein 2. Although genetic testing can lead to the identification of genetic variation which can predispose to AMD, the complex pathogenesis of
6715-401: The retina, and in geographic atrophy, there are three specific layers that undergo atrophy: the choriocapillaris, retinal pigment epithelium, and the overlying photoreceptors. The three layers that undergo atrophy in geographic atrophy are all adjacent to each other. The photoreceptors are the most superficial and they are the cells that are responsible for converting energy from the light from
6800-479: The risk of developing glaucoma. A study with 1636 persons aged 40-80 who had an intraocular pressure above 24 mmHg in at least one eye but no indications of eye damages showed that after five years 9.5% of the untreated participants and 4.4% of the treated participants had developed glaucomatous symptoms, meaning that only about one in ten untreated people with elevated intraocular pressure will develop glaucomatous symptoms over that period of time. Therefore, it
6885-508: The systemic safety of bevacizumab and ranibizumab are similar when used to treat neovascular AMD, except for gastrointestinal disorders. Bevacizumab however is not FDA approved for treatment of macular degeneration. A controversy in the UK involved the off-label use of cheaper bevacizumab over the approved, but expensive, ranibizumab. Ranibizumab is a smaller fragment, Fab fragment, of the parent bevacizumab molecule specifically designed for eye injections. Other approved antiangiogenic drugs for
6970-412: The treatment of neo-vascular AMD include pegaptanib and aflibercept . These anti-VEGF agents may be administered monthly or adaptively. For adaptive anti-VEGF treatment, two approaches are conventionally applied. In the case of pro re nata , the patient comes at fixed intervals, but treatment is only administered if an activity is detected (i.e., presence of fluid). In the case of treat-and-extend ,
7055-437: The wet form, anti–vascular endothelial growth factor injected into the eye or, less commonly, laser coagulation or photodynamic therapy may slow worsening. Dietary antioxidant vitamins , minerals , and carotenoids do not appear to affect the onset; however, dietary supplements may slow the progression in those who already have the disease. Age-related macular degeneration is a main cause of central blindness among
7140-510: The working-aged population worldwide. As of 2022, it affects more than 200 million people globally with the prevalence expected to increase to 300 million people by 2040 as the proportion of elderly persons in the population increases. It affects females more frequently than males, and it is more common in those of European or North American ancestry. In 2013, it was the fourth most common cause of blindness, after cataracts , preterm birth , and glaucoma . It most commonly occurs in people over
7225-536: Was to get to those layers, many free radicals would form and cause damage to nearby tissues. The deepest layer that undergoes atrophy in geographic atrophy is called the choriocappilaris. It is a capillary network that provides nutrients to the retinal pigment epithelium. The pathophysiology of geographic atrophy is still uncertain. Some studies questioned whether it was due to a deficient retinal pigment epithelium, leading to increased oxidative stress. Other studies have looked for inflammatory causes of damage. Thus far,
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