A retinal tear or break happens when the gel-like vitreous in your eye pulls on your retina and causes a split. Your retina is a thin layer of tissue that’s sensitive to light found at the back of your eye.
A retinal tear isn’t the same as a retinal detachment. A retinal tear could lead to a retinal detachment if the tear isn’t treated. A retinal detachment happens when the retina pulls away from the tissues that support it.
You can also develop a hole in your retina when your retina gets thinner. Retinal holes are less likely to lead to retinal detachment.
Retinal tears and any injury that damages your retina threatens your eyesight and is a medical emergency. Contact your eye care provider as soon as you have retinal tear symptoms or any type of eye injury.
How common is a retinal tear?
Retinal tears are common, with nearly one in ten people developing one at some point during their lifetime. Retinal detachments, on the other hand, are less common, occurring in approximately one in 300 people.
Can stress cause a retina tear?
Even though stress can't cause retinal detachment, it can be harmful to your eye health in other ways. In addition to cortisol during times of stress, the body also produces epinephrine or adrenaline. This causes the pupils to dilate so you are able to see the world more clearly and be protected from danger.
A retinal tear is less severe than a retinal detachment, but you still may need treatment. You probably won’t feel pain, but you may have blurry vision and a lot of eye floaters and light flashes. Your provider can repair a tear before it leads to a detached retina.
What are the symptoms of a retinal tear?
Symptoms of a retinal tear may include:
Flashes of light (photopsia).
Suddenly seeing more black spots or floaters than usual.
Darkening vision.
Blurred vision.
You might have a retinal tear and have no symptoms.
Leber congenital amaurosis (LCA) is a rare, inherited eye disorder that causes severe vision loss from birth or early childhood. It's the most common cause of inherited childhood blindness. LCA affects the retina, specifically the photoreceptor cells (rods and cones) responsible for detecting light and color, leading to severe vision impairment.
Leber’s congenital amaurosis is a rare eye disease that affects babies’ retinas. Some babies have blindness at birth. Others have very poor vision. Changes in genes that develop and form retinas cause Leber’s congenital amaurosis. Treatment for children with very poor vision includes eyeglasses or magnifying glasses.
Pulsatile blood flow in the central retinal artery
Some babies with LCA are born with blindness. Other babies with the condition develop symptoms when they’re about 6 months old. You may not notice any changes in your baby’s vision right away. For example, babies often rub their eyes when they’re tired. But your baby frequently rubbing or poking at their eyes may be an early symptom of LCA. Other symptoms include:
Misaligned eyes (strabismus)
Sensitivity to light (photophobia)
Shaking eyes (nystagmus)
Your child’s pupils don’t adjust to changes in light (slow or missing pupillary response)
People with LCA typically experience very poor vision from birth or early infancy, often with vision worse than 20/400 (meaning they can only see at 20 feet what someone with normal vision can see at 400 feet). Some individuals may have only light perception or no vision at all.
One of the factors that affects your child’s eye development and visual function is the genes they inherit from each parent. Normal genes will work together to create a functioning eye. Unfortunately, abnormal genes can be passed on and can disrupt your child’s eye development. In Leber’s Congenital Amaurosis, mutated genes cause the retina to develop improperly and can lead to severe vision loss or blindness.
Leber’s Congenital Amaurosis is a disease in which the retina of affected infants develops incorrectly, leading to severe visual impairment.
LCA is one of multiple inherited retinal diseases and must be passed down by both parents for the child to have it.
The genes responsible for LCA can be detected in parents and their children with specialized testing and are part of how children are officially diagnosed with LCA.
Visual aids can help children adapt to their level of vision loss, and support groups help parents and children deal with the realities of LCA.
Several clinical trials using gene therapy have shown promising results for helping stop LCA progression.
LCA causes
Leber’s congenital amaurosis happens when your baby inherits certain genetic variations that affect how their retinas develop.
The genetic variations affect the process that creates images that your baby sees. Normally, light-detecting cells (photoreceptors) in your baby’s retinas turn light into electrical signals. Your baby’s brain turns the signals into images that they see. Leber’s congenital amaurosis affects that process so there’s less electrical activity (signals). The less electrical activity there is, the less sight your baby has.
Variations in almost 30 different genes can cause Leber’s congenital amaurosis. The variations affect the following genes:
CEP290
CRB1
GUCY2D
RPE65
LCA is usually an autosomal recessive condition. That means both biological parents have one or more of the changed genes that can cause Leber’s congenital amaurosis.
Diagnosis:
Early detection: Parents may notice a lack of visual response in the first few months of life.
Electroretinogram (ERG): This test measures the electrical activity of the retina and can help confirm LCA.
Genetic testing: Can help identify specific gene mutations causing LCA.
Metamorphopsia is vision dysfunction that causes objects — specifically straight lines — to appear warped, distorted or bent. Rather than a condition itself, metamorphopsia is a symptom. It can result from brain conditions or when there’s a problem with the macula, which is the center of the retina.
somesthetic distortions, including:
Macropsia: Objects appear larger than they are
Micropsia: Objects appear smaller
Teleopsia: Objects seem farther away
Pelopsia: Objects seem closer
Metamorphopsia: Patients perceive their body or body parts as enlarging or shrinking
Chromatopsia: Altered perception of colors
What is metamorphopsia in medical terms?
The term metamorphosis means to change a form or shape of nature into a completely different one. The prefix meta- means after or beyond, the combining form -morph/o means shape and the suffix -sis means an abnormal condition or process.
Metamorphopsia (“meta-more-FOP-see-ya”) is a medical term used to describe an abnormal visual perception in which images appear distorted. For example, straight lines appear curved or jagged. It is an important symptom of retinal disease. Metamorphopsia is not caused by the need for new glasses, cataract, glaucoma, or optic nerve damage. Metamorphopsia is a sign of a retinal problem. It is detected and monitored with an Amsler grid.
Metamorphopsia. Metamorphopsia (from Ancient Greek: μεταμορφοψία, metamorphopsia, 'seeing mutated shapes') is a type of distorted vision in which a grid of straight lines appears wavy or partially blank. In addition, metamorphopsia can result in misperceptions of an object's size, shape, or distance to the viewer.
The retina is a thin layer of tissue at the back of the eye that uses light to create signals. Signals are sent to the brain through the optic nerve, and registered as an image. The macula is in the middle of the retina and gives us color vision, central vision and visual acuity.
When the retina or macula are affected by age, trauma or disease, metamorphopsia can result. It may affect one or both eyes and may only involve a portion of the vision in the affected eye. Metamorphopsia can potentially indicate the presence of a serious underlying medical cause.
What does metamorphopsia look like?
Metamorphopsia affects central vision. This means objects in your peripheral vision will likely appear normal, while things in front of you are distorted. While metamorphopsia is a symptom in itself, some signs to look out for include:
Objects that are normally straight appear curved or warped. Example: A light pole looking bent or “melted.”
Things that are normally flat appear rounded. Example: A frisbee looking like a bowl.
Borders on objects appear smudged or distorted. Example: The face of a watch looks like someone smeared the edges of it.
Objects change shape. Example: A rectangular door frame twists out of shape.
Things look disproportionately larger than normal (macropsia).
Things look disproportionately smaller than normal (micropsia).
If you experience any of the symptoms listed above without explanation, seek help from an eye doctor or medical professional.
How is metamorphopsia diagnosed?
Your eye doctor may run a series of tests to determine whether you have metamorphopsia and how severe it is. The tests usually involve having the patient look at some type of chart and answering questions about what they see. Some tests used to measure metamorphopsia include:
Amsler grid
Amsler grid for metamorphopsia is the most well-known and the most commonly used test that doctors use. It involves looking at a box with equally spaced horizontal and vertical lines that create a grid. In the middle of the grid is a small dot.
To take the test, the patient must be wearing corrective lenses, reading glasses or whatever is required for them to have their best corrected vision. Then, they focus on the dot in the middle of the grid while covering one eye at a time. This part is especially important, as looking at the grid with both eyes can cause the good eye to compensate for the bad eye.
While focusing on the dot in the middle, the patient should pay attention to how the lines around the dot appear. If they still appear straight, metamorphopsia isn’t the problem. If these lines appear curved or warped, metamorphopsia may be the problem.
A patient’s perspective of metamorphopsia (B) compared to normal (A)
M-chart
The M-chart is more specific than the Amsler grid, but it isn’t used as often. It was created to help pinpoint the degree of metamorphopsia and whether the distortion is more present in horizontal or vertical lines.
The test has 19 dotted lines, starting with a straight line (zero degrees). The size and space between the dots that create the line gradually go from very fine (0.2 degrees) to coarse (2.0 degrees). Each line has a dot in the middle of it that the patient is supposed to focus on.
Starting with the straight, solid line, the patient will focus on the dot and tell the doctor whether the line looks curved in places or not. They do this for every line, from fine to coarse, until the line no longer looks distorted to the patient.
Once this is recorded, the doctor will turn the M-chart 90 degrees (making vertical lines horizontal or vice versa). The patient will perform the test again. eResearch by Navid Ajamin -- winter 2025
The farther the patient goes before the line no longer looks curved, the more severe their metamorphopsia is. It’s also recorded whether vertical or horizontal lines are affected more than the other.
Possible Causes
What are the most common causes of metamorphopsias?
Depending on why they happen, metamorphopsias can be a minor annoyance or a sign of serious problems. There are three main sources of metamorphopsias:
Refraction conditions and changes (most common).
Retinal changes and conditions.
Brain-related conditions (least common).
Metamorphopsia can be a symptom of a number of eye disorders involving the retina or macula.
Some of these conditions include the following:
Age-related macular degeneration
Epiretinal membrane and vitreomacular traction
Posterior vitreous detachment
Macular hole
Refraction conditions and changes
Your eye bends (refracts) light as it enters and passes through. That bending is supposed to focus light beams precisely on your retina. The more precise the focus, the clearer you see. Refractive errors are when that refracting doesn’t happen correctly. Examples include:
Strong or severe refractive errors like astigmatism.
A large difference in prescription strength needs between your eyes (anisometropia).
Cornea or lens shape changes/differences.
New corrective lenses (like eyeglasses or contacts), especially with bigger changes to how you see.
What Is the Amsler Grid
Retinal changes and conditions
The retina at the back of your eye has a light-detecting layer of cells (photoreceptors). Part of how they work is due to the shape of your retina, which needs to lay flat against the layer underneath.
Wrinkles, holes or other retinal changes can cause metamorphopsias when they change the shape or position of your retina. Metamorphopsias are more severe when they happen in the macula, the part of your retina responsible for detecting color and fine details.
Your retina needs light to arrive with precise timing, so changes in your retina’s shape distort what you see if the light arrives too early. And if the changes in your retinal shape or position are severe, it can destroy the connections that let your retinas send light-related signals to your brain. When that happens, it can cause permanent vision loss or even blindness.
Retinal and retina-related conditions that can cause metamorphopsias include:
Age-related macular degeneration, especially the wet form.
Central serous retinopathy.
showing the visual perception
Chorioretinopathy conditions like chorioretinitis.
Cystoid macular edema.
Diabetes-related retinopathy and diabetes-related macular edema (swelling).
Macular pucker.
Ocular migraine.
Retinal bleeding (hemorrhage).
Retinal tears or detachments.
Retinitis pigmentosa.
Uveitis, including choroid inflammation from infection-related conditions like presumed ocular histoplasmosis syndrome.
Retinoschisis is a condition that happens when your retina divides into two or more layers. Schisis means a split or a cleft. Retinoschisis affects the light-sensing layer of your retina and the layer of cells that transmits signals to your brain through the optic nerve.
This division of the layers can affect how well you see. Splits can occur in the center of the retina but are more likely at the periphery (outer edges).
What are the signs and symptoms of retinoschisis?
You may have no symptoms of the disease. If you do, symptoms that may happen with juvenile X-linked retinoschisis include:
Eyes that turn toward your nose (crossed eyes).
Eyes that move uncontrollably from one side to the other (nystagmus).
Loss of central (foveal) vision or side (peripheral) depending on where the split occurs.
Having farsightedness.
If you’ve developed acquired retinoschisis, you might find that you can’t see clearly on either side (loss of peripheral vision). You may not have any symptoms at all.
If you have retinoschisis and it becomes severe, or you also have retinal detachment, you may notice:
Floaters and flashers.
Distorted images.
Loss of central (foveal) vision or side (peripheral) depending on where the split occurs.
Are X-linked disorders male or female?
X-linked recessive diseases most often occur in males. Males have only one X chromosome. A single recessive gene on that X chromosome will cause the disease. The Y chromosome is the other half of the XY gene pair in the male.
Patterns of inheritance
Patterns of X-linked recessive inheritance in a royal family
In humans, inheritance of X-linked recessive traits follows a unique pattern made up of three points.
The first is that affected fathers cannot pass X-linked recessive traits to their sons because fathers give Y chromosomes to their sons. This means that males affected by an X-linked recessive disorder inherited the responsible X chromosome from their mothers.
Second, X-linked recessive traits are more commonly expressed in males than females.This is due to the fact that males possess only a single X chromosome, and therefore require only one mutated X in order to be affected. Women possess two X chromosomes, and thus must receive two of the mutated recessive X chromosomes (one from each parent). A popular example showing this pattern of inheritance is that of the descendants of Queen Victoria and the blood disease hemophilia.
The last pattern seen is that X-linked recessive traits tend to skip generations, meaning that an affected grandfather will not have an affected son, but could have an affected grandson through his daughter. Explained further, all daughters of an affected man will obtain his mutated X, and will then be either carriers or affected themselves depending on the mother. The resulting sons will either have a 50% chance of being affected (mother is carrier), or 100% chance (mother is affected). It is because of these percentages that we see males more commonly affected than females.
X-Linked Retinoschisis (XLRS)
A rare disorder involving multiple structure of the eye characterized by reduced visual acuity in males due to juvenile macular degeneration. Clinical features such as vitreous hemorrhage, retinal detachment, and neovascular glaucoma can be observed in advanced stages.
X-linked Retinoschisis or X-Linked Juvenile Retinoschisis is a rare congenital disease of the retina caused by mutations in the RS1 gene, which encodes retinoschisis, a protein involved in intercellular adhesion and likely retinal cellular organization.
X-linked retinoschisis, with a prevalence of about 1 in 15,000 to 30,000, is one of the main causes of juvenile macular degeneration in males. It is characterized by symmetric bilateral macular involvement beginning in the first decade of life.
X-linked recessive genetic defects
It is caused by a large variety of mutations in theRS1 gene on Xp22.1-p22.3, which encodes the protein retinoschisis. This protein is involved in intercellular adhesion and likely retinal cellular organization. X-linked retinoschisis is inherited in an X-linked manner with complete penetrance and variable expressivity.
Most affected individuals are males, as heterozygous females are rarely affected. However, retinoschisis has been reported in non-consanguinous females. The phenotype can be markedly variable even within the same genotype and can involve the peripheral retina.
اشتارگات (به انگلیسی: Stargardt disease) یک بیماری ژنتیک نادراست که باعث اختلال بینایی در مرکز شبکیه چشم میشود.
Stargardt disease is the most common form of inherited juvenile macular degeneration, occurring in one in every 8,000 to 10,000 people worldwide. It causes gradual loss of central vision. It usually develops during childhood or adolescence, resulting in a loss of the central part of the visual field.[2]
عوامل ایجاد بیماری[1]
بیماری اشتارگارت یک مشکل مدیریت پسماند است، عامل ایجاد این بیماری نادر جهش در ژن ABCA4 میباشد، به این صورت که هم پدر و هم مادر باید حامل این ژن باشند تا به فرزند منتقل شود.
معمولاً در ازدواجهای فامیلی این جهش مشهود هست. دو نوع جهش ABCA4 موجود است.
در این جهشها سنتز ویتامین A مختل میشود و باعث تجمع پسامد در روی شبکیه شده و گیرندههای نوری سطح شبکیه را مختل میکند. ویتامین A یک عنصر مهم برای گیرندههای نوری سطح شبکیه چشم هستند.
Stargardt Disease: What It Is, Symptoms & Treatment
Stargardt disease is an inherited form of macular degeneration that first appears in childhood or adolescence. It is characterized by progressive vision loss beginning in the macula, the central part of the retina where light falls and visual acuity and color vision are greatest. Symptoms include blurred or wavy vision, blind spots, impaired color vision, and difficulty seeing in low light situations. People with Stargardt disease are usually sensitive to glare.[2]
What are symptoms of Stargardts eye disease[3]
Someone may initially become aware of an issue with their center vision. It may be distorted, hazy, or have black regions. Side vision (peripheral vision) is frequently unaffected. Colorblindness is a condition in which some individuals have difficulty perceiving colors.
When moving between bright and dark environments, eyesight may take longer to adapt than normal.
For some patients, Stargardt illness advances slowly at first, then quickly accelerates and finally plateaus. Vision loss may accelerate at roughly 20/40 vision (meaning someone sees at 20 feet what a normal-seeing person sees at 40 feet).
While most persons with Stargardt illness eventually lose their central vision, many may have strong side vision for the remainder of their lives. eResearch by Navid Ajamin -- autumn 2024
What can be done if Stargardt disease is diagnosed?There is no cure for Stargardt disease, and there are no treatments.
What devices can help?Since the symptoms are underlying physiology of Stargardt disease are similar to those for other types of macular degeneration, people can usually benefit from the same devices as used for age-related macular degeneration (AMD). These help people retain independence in their homes, school, and jobs. Products include electronic magnifiers and devices that turn text into speech to read aloud mail, bills, books, and other printed materials. Freedom Scientific’s line of video magnifiers and screen magnification software can help.[2]
اشتارگات معمولا در کودکان، نوجوانان و بزرگسالان جوان ایجاد می شود. ممکن است شخصی ابتدا متوجه مشکلی در بینایی مرکزی خود شود. این مشکل معمولا تاری دید یا مشاهده نواحی تیره است. در این نوع بیماری چشمی دید جانبی یا محیطی معمولاً تحت تأثیر قرار نمی گیرد. اما برخی از افراد ممکن است در دیدن رنگ ها نیز مشکل داشته باشند. بیماری اشتارگات در برخی افراد ممکن است به کندی پیشرفت کند، سپس سرعت گیرد و به سرعت سطح بینایی را به میزان قابل توجهی کاهش دهد. با توجه به اینکه در بیماری اشتارگات از دست دادن بینایی می تواند به صورت ناگهانی سرعت خود را افزایش دهد، بنابراین در صورتی که با علائم اولیه مانند تاری دید یا مشاهده نواحی تیره مواجه شدید، باید سریعا به پزشک مراجعه کنید.
تغییر در بینایی مرکزی Central vision معمولاً منجر به تشخیص اولیه بیماری اشتارگات می شود. یک پزشک متخصص شبکیه چشم در حال معاینه شبکیه یک فرد مبتلا به بیماری اشتارگات ، لکه های زرد رنگ مشخصی را در RPE مشاهده می کند. لکه ها رسوبات لیپوفوسسین هستند که محصول جانبی فعالیت طبیعی سلول های شبکیه می باشند. با این حال، در این بیماری، لیپوفوسین به طور غیر طبیعی تجمع می یابد.
نکته: “توجه داشته باشید که پیشرفت از دست دادن بینایی در بیماری اشتارگات متغیر است. حدت بینایی (قابلیت تشخیص جزئیات و شکل) ممکن است در ابتدا به آرامی کاهش یابد، سپس شتاب بگیرد و دوباره یکنواخت شود. همچنین معمولاً مقداری دید محیطی در فرد مبتلا باقی خواهد ماند.”
? Can people with Stargardts drive
معمولاً بیماری اشتارگات از والدین منتقل می شود. در این بیماری، ژنهای معیوب (ژن ABCA4) برای داشتن علائم باید از هر دو والدین منتقل شود. هر کودک ۲۵ درصد ممکن است دو نسخه ABCA4 (یک نسخه از هر والدین) را که برای ایجاد این بیماری لازم است، به ارث ببرد. فردی که این ژن را فقط از یکی از والدین دارد، ناقل بیماری اشتارگات خواهد بود، اما علائمی نخواهد داشت. البته سایر اشکال بیماری اشتارگات برای ایجاد علائم تنها به ژن یکی از والدین نیاز دارند، اما این موارد بسیار نادر هستند. برای تشخیص دقیق این بیماری چشم پزشک معمولا از آزمایشی به نام آنژیوگرافی فلورسین استفاده می کند. در این آزمایش یک رنگ به بازوی شما تزریق می شود. از رنگ هنگام گردش در رگ های خونی شبکیه عکس گرفته می شود. در افراد مبتلا به اشتارگات عکس ها ناحیه تیره ای را در بافت شبکیه نشان می دهند. این به چشم پزشک کمک می کند تا بیماری اشتارگات را تشخیص دهد. همچنین در حال حاضر آزمایش ژنتیک برای تشخیص دقیق نوع دژنراسیون ماکولا در دسترس است. این مطمئن ترین راه برای دانستن مبنای ژنتیکی بیماری شما است.
بهترین گزینه برای جلوگیری از ابتلای فرزندان به بیماری اشتارگات انجام آزمایش ژنتیک است که به والدین در تشخیص قطعی بیماری و احتمال خطر ابتلای فرزندان به این بیماری کمک می کند. البته تا به امروز متاسفانه هیچ درمانی برای این بیماری وجود نداشته است. اما با این وجود چندین آزمایش ژن درمانی و دارودرمانی در حال انجام است. در ادامه به برخی از نکاتی که به افراد مبتلا به بیماری اشتارگات کمک می کند.
خوشبختانه اشتارگات یک بیماری ژنتیکی و نادر است که اغلب در کودکان تشخیص داده میشود. این بیماری به علت اشکال در ساختارهای استخوانی و بافتی در بدن ایجاد میشود. افراد مبتلا به اشتارگات ممکن است دارای قد کوتاهی، مشکلات در مفاصل و اندامهای حرکتی، اختلالات تنفسی، و مشکلات قلبی باشند. اشتارگات نیازمند مراقبت و مدیریت تخصصی پزشکی است. درمان این بیماری شامل جراحیها، فیزیوتراپی، و مراقبتهای پزشکی مخصوص میشود. ارتقاء کیفیت زندگی افراد مبتلا به اشتارگات از طریق تیمهای درمانی و پشتیبانی اجتماعی انجام میشود تا به افراد این امکان داده شود تا با این بیماری مبارزه کنند و به حیات عادی نزدیکتر شوند.
درمان
سلول بنیادی
درمان قطعی برای بیماری اشتارگات در حال حاضر وجود ندارد، اما بیماری به وسیله ژن درمانی و سلول درمانی به وسیله سلولهای بنیادی قابل کنترل است و احتمال بهبود بیماری با ضریب بیشتری بالا میرود، استفاده از سلولهای بنیادی بستگی به زنده ماندن سلولهای بنیادی در محیط شبکیه چشم دارد، گاهی نیاز است در مقاطع زمانی مختلف درمان تکرار شود.
ویتامین آ
دانشمندان با جایگزین کردن اتمهای هیدروژن با دوتریوم Deuterium در ویتامین A توانستند Alk-001 را تولید کنند. این محصول که به عنوان ویتامین A دوتره (Deuterated Vitamin A) شناخته میشود، اصطلاحاً پاکتر از شکل طبیعی ویتامین A میسوزد. دوتریوم (Deuterium)، شکل بی خطری از هیدروژن است که بهطور طبیعی در بدن انسان تولید شده و غیر رادیواکتیو است. Alk-001 هماکنون در محله سوم کارآزمایی بالینی در بیماری اشتارگارت میباشد. . نام علمی Alk-001 عبارت است از C20-D3- retinyl . .acetate
شبکیه مصنوعی
جدیدترین تکنولوژی برای درمان بیماران شبکیه چشم، استفاده از شبکیه مصنوعی یا شبکیه الکترونیکی است. این تکنولوژی در سال ۲۰۱۶ ابداع شد، هرچند کیفیت تصویر بهدست آمده برای بیمارن چندان واضح نبود، اما پروژه شبکیه مصنوعی در حال ارتقا کیفیت است.
This disease is hereditary and therefore if there is a family history it is wise to be attentive, even though this does not mean that the disease is sure to manifest itself. Approximately 90% of cases are transmitted in an autosomal recessive manner, i.e. both parents must have the affected gene and this is often very hard to establish. In this case, the possibility of a boy or girl having the disease is 25% and it should be remembered that 10% of cases, with a family history, are of dominant inheritance.As it is a recessive gene, the family history of the disease may not be known or available. This is why it is necessary to pay special attention to the initial symptoms e.g. if children or adolescents find difficulty in reading or watching the television. At these ages, it is a good idea to explain the pathology to them so that they can be made aware of what will happen to them, can adapt to the situation and can lead a happy life.Stargardt’s disease causes out-of-focus vision that lacks sharpness. This makes it difficult to recognise faces and read both nearby and at a distance. As a result, colours with a similar shade (for example, red and green or blue and yellow) look alike.
A 40-year-old man experiencing decreased vision (visual acuity: 0.8) and dyschromatopsia in both eyes with Stargardt disease. A and B: The fundus photos of the right and left eyes respectively reveal the bull's eye maculopathy characterized by paracentral RPE depigmentation and atrophy, as well as pisiform, round, or dot-like yellow-white flecks. C and D: The red-free fundus images of the right and left eyes. E and F: OCT macula scans of the right and left eyes respectively, highlighting photoreceptor layer disorganization. (Courtesy of J. Khadamy) [5]
STARGARDT FINDINGS. (1A,1B) Fundus photography shows bilateral atrophic macular changes surrounded by diffuse pisciform flecks. (2A,2B) Fluorescein angiography reveals a dark choroid with hyperfluorescent pisciform flecks.[6]
A good knowledge of the disease helps sufferers to understand what is happening to them, adapt their lives to the new situation and take some recommended measures like using sunglasses with u/v protection and avoiding supplements that contain vitamin A.
In the field of research into treatments for this disease, science is progressing. The clinical trials and European projects in which the Barcelona Macula Foundation and the Institut de la Màcula participate in collaboration with leading international research centres are essential and lead to hope that the disease may be treatable in the future.[4]
یکسلول گیرنده نور(photoreceptor) نوع خاصی از سلول موجود در شبکیه است که قادر به انتقال نور فضا است. اهمیت بیولوژیکی فتوریسپتورها این است که آنها نور (تابش الکترومغناطیس قابل مشاهده) را به سیگنالهایی تبدیل میکنند که میتوانند فرایندهای بیولوژیکی را تحریک کنند.برای مشخص شدن بیشتر، پروتئینهای فتوریسپتور در سلول، فوتونها را جذب کرده و موجب تغییر در پتانسیل غشاء سلولی میشوند.
انواع گيرنده هاي نوري
سلولهاي مخروطي به طور كلي نقش مهمتري در انجام وظايف بينايي داشته و بهتر از سلولهاي استوانه اي عمل میکنند (بجز شناسايي تحريكات نور ضعيف).
دقت بينايي منتقل شده توسط سلولهاي مخروطي از دقت بينايي كه توسط سلولهاي استوانهاي منتقل مي شود بيشتر است و سلولهاي مخروطي تفكيك بهتري از تغييرات سريع تصوير بينايي را فراهم مي كنند (قابليت تفكيك بهتر تغييرات نور در زمان).
سلولهاي مخروطي ديد رنگي را نيز منتقل مي كنند. سيستم سلولهاي استوانهاي در برابر نور، حساسيت بيشتري از سيستم مخروطي دارد. اما اين سيستم فاقد رنگ است.اين تفاوتها در عملكرد، ناشي از مشخصات خودسلولهاي مخروطي و استوانهاي و همچنين مربوط به ارتباطاتي است كه توسط اين سلولها با ديگر نورونها در شبكيه برقرار مي شود.[1]
A photoreceptor cell is a specialized type of neuroepithelial cell found in the retina that is capable of visual phototransduction. The great biological importance of photoreceptors is that they convert light (visible electromagnetic radiation) into signals that can stimulate biological processes. To be more specific, photoreceptor proteins in the cell absorb photons, triggering a change in the cell's membrane potential.
There are currently three known types of photoreceptor cells in mammalian eyes:
rods, cones, and intrinsically photosensitive retinal ganglion cells.
The two classic photoreceptor cells are rods and cones, each contributing information used by the visual system to form a representation of the visual world, sight. The rods are narrower than the cones and distributed differently across the retina, but the chemical process in each that supports phototransduction is similar.
A third class of mammalian photoreceptor cell was discovered during the 1990s: the intrinsically photosensitive retinal ganglion cells. These cells do not contribute to sight directly, but are thought to support circadian rhythms and pupillary reflex.[2]
Difference between rodsand cones
Rods and Cones are the photoreceptors, useful in providing vision to the eyes. Rods provide vision during dim light or night also known as scotopic vision, whereas cones provide vision during day time or at bright light also known as photopic vision. Secondly, rods do not support the colour vision, but cones are capable of colour vision, with high spatial acuity — the level of the light where both the types of work, is called a mesopic vision. eResearch by Navid Ajamin -- spring 2019
There are around 125 million photoreceptors present in the human eye, and these cells work by absorbing light and further converting into signals, which triggers the membrane potential and result in visual phototransduction or supporting the vision in the light.
There are various factors like sensitivity, function, deficiency disease, etc. to differentiate the rods and cones, with this article we will focus on such points and the brief description of them.[3]
Comparison of human rod and cone cells,[2]from Eric Kandel et al. in Principles of Neural Science.
Cones
Rods
Used for photopic vision (vision under high light conditions)
Used for scotopic vision (vision under low light conditions)
Not very light sensitive; sensitive to only direct light
Very light sensitive; sensitive to scattered light
Loss causes legal blindness
Loss causes night blindness
High visual acuity; better spatial resolution
Low visual acuity
Concentrated in fovea
Not present in fovea
Fast response to light, can perceive more rapid changes in stimuli
Slow response to light, stimuli added over time
Have less pigment than rods, require more light to detect images
Have more pigment than cones, so can detect lower light levels
Disks are attached to outer membrane
Stacks of membrane-enclosed disks are unattached to cell membrane directly
About 6 million cones distributed in each retina
Three types of photosensitive pigment in humans
Confer color vision
About 120 million rods distributed around the retina
One type of photosensitive pigment
Confer achromatic vision
A number of eye problems can involve photoreceptor cells.
These problems include:
Color blindness ,Photokeratitis ,Retinitis pigmentosa, Usher syndrome [4]
CONES
Rods
BASIS FOR COMPARISON
[3]
Cones are also photoreceptors present in the eye, they are fewer in number and are of the cone shape.
Rods are one of the photoreceptors found in the eye, these have rod-like structure and provides twilight vision.
Meaning
Cones are usually located in the center of the retina.
Rods are usually located around the boundary of the retina.
Location
Cones are 5 million photoreceptors.
Rods are about 120 million photoreceptors out of the total 125 million photoreceptors in the human eye.
Amount
The outer segment is conical of Cones which contain iodopsin pigment.
The outer segment is cylindrical of Rods which contain rhodopsin pigment, made up of Vitamin A.
The shape of the outer segment/Pigment
Cones give colour vision, and they are of three types: green, blue, and red.
Rods cells do not give colour vision, and they do not have any differentiation.
Colour vision
Lack of the pigment in the cones, known as iodopsin may cause colour blindness.
Lack of the pigment in the rods, known as rhodopsin may cause night blindness.
Disease/Deficiency
Fundamentals of the retinal visual cycle
To reach the retina, light passes first through the cornea, the aqueous humour, the crystalline lens and then the vitreous humour. From here, it crosses the retinal ganglion cells and then several cell layers before reaching the outer retina. The outer retina is composed of retinal pigment epithelium (RPE) cells plus the outer segments of the visual photoreceptors (rods and cones)
Schematic representation of the major retinal cell types and their organization in the retina. The outermost part of the retina is the retinal pigment epithelium (RPE), which consists of a monolayer of cuboid, pigmented cells between the photoreceptors and the choroid. The retina is divided into three laminar layers: the outer nuclear layer (ONL), the inner nuclear layer (INL), and the ganglion cell layer (GCL). The nuclei of rod and cone photoreceptors are located in the ONL. The INL comprises the nuclei of the bipolar, horizontal, and amacrine cells. Cell bodies of the retinal ganglion cells are present in the GCL, and their axons form the nerve fiber layer (NFL), just beneath the GCL. Synapses between photoreceptors and interneurons are located in the outer plexiform layer (OPL) and interneurons synapse with RGC in the inner plexiform layer (IPL). Müller cells span all retinal layers. Microglia are mainly found in IPL and GCL, whereas astrocytes are located near the NFL.[5]
Light moves through the eye and is absorbed by rods and cones at the back of the eye.[6]
Age-related macular degeneration (AMD) is a medical condition which usually affects older adults and results in a loss of vision in the center of the visual field (the macula) because of damage to the retina. It occurs in “dry” and “wet” forms. It is a major cause of blindness and visual impairment in older adults (>50 years). Macular degeneration can make it difficult or impossible to read or recognize faces, although enough peripheral vision remains to allow other activities of daily life.[1]
Age-related macular degeneration (AMD) is an eye disease that can blur your central vision. It happens when aging causes damage to the macula — the part of the eye that controls sharp, straight-ahead vision. The macula is part of the retina (the light-sensitive tissue at the back of the eye).[9]
Dry macular degeneration, also known as atrophic or non-neovascular age-related macular degeneration (AMD), is a common eye condition that primarily affects the macula, the central part of the retina responsible for sharp, central vision. In dry AMD, there is a gradual breakdown or atrophy of the light-sensitive cells in the macula, particularly the retinal pigment epithelium (RPE) cells. These cells are crucial for supporting the health and function of the photoreceptor cells, including cones, in the macula.
The condition progresses slowly over time and can lead to symptoms such as blurred central vision, distorted vision (metamorphopsia), and difficulty seeing in low light. Unlike wet AMD, which involves abnormal blood vessel growth, dry AMD typically does not involve leaking blood vessels.
There are two main types of dry macular degeneration:
Early and Intermediate Dry Macular Degeneration: In the early stages, small yellow deposits known as drusen may form beneath the retina. Drusen are accumulations of waste materials that can interfere with the normal functioning of the macula. At this stage, individuals may not experience significant vision loss, and the condition may be detected during a routine eye exam.
Advanced Dry Macular Degeneration (Geographic Atrophy): Over time, some individuals with dry AMD may progress to an advanced stage characterized by the development of geographic atrophy. Geographic atrophy involves the loss of RPE cells and photoreceptor cells in discrete patches, leading to the formation of atrophic or “geographic” areas in the macula. This can result in a more significant and irreversible loss of central vision.[8]
Macular Degeneration - Symptoms and Detection Symptoms of Dry AMD include the presence of drusens that begin to enlarge. Another symptom is blurry areas in central vision. A symptom of Wet AMD is seeing straight lines as wavy ones.
A visual acuity test can help an eye care professional determine if any central vision is lost. An Amsler grid may also be used to detect AMD. In this test you cover one eye and stare at a black dot that has patterns of straight lines. If these lines appear wavy or are missing then AMD could be present.[2]
Prevention
There is growing evidence that by improving your diet, you may also improve the health of your eyes. Research has suggested an association between macular degeneration and a high saturated fat diet.
There is also evidence that eating fresh fruits and dark green, leafy vegetables – foods rich in vitamins C and E, selenium, and carotenoids (including beta-carotene, lutein and zeaxanthin) – may delay or reduce the severity of AMD.
How AMD can affect your sight?
AMD is progressive and it is also painless. While AMD may affect your central vision, most people still retain useful side (or peripheral) vision. Key symptoms of AMD include:
Distortion, where straight lines may appear wavy or bent. For example, lines of tiles in the bathroom appear wavy.
Difficulty in reading or doing any other activity which requires fine vision.
Difficulty in distinguishing faces.
Dark patches or empty spaces, which appear in the centre of your vision.
The need for increased illumination, sensitivity to glare, decreased night vision and poor colour sensitivity.[6]
Foods to Enjoy eResearch by Navid Ajamin -- spring 2012
Eat the freshest and brightest fruits and vegetables. Pick the most colorful vegetables and fruits you can find - red, dark green, orange, or yellow. These foods play a key role in keeping your eyes healthy:
Carrots Corn Kiwi Pumpkin Yellow squash Zucchini squash Red grapesGreen peas Cucumber Butternut squash Green bell pepper Celery Cantaloupe Sweet potatoes Dried apricots Tomato and tomato products Dark green leafy vegetables SpinachKaleTurnips Collard greens ...
Fish
Eating fatty fish such as salmon, tuna or mackerel two to three times per week can slow the progression of age-related macular degeneration (AMD) according to a study published in the British Journal of Ophthalmology.
This research further confirms earlier studies that suggested eating fish can help reduce the risk of getting AMD and demonstrates that some of those already affected by the disease can benefit as well.
Nuts
Nuts not only contain Omega-3 fatty acids, but also copper which can play a role in preventing age-related eye diseases. Even just a handful of nuts at two or three times a week can reduce your risk of AMD.
Foods to Avoid
A high-fat, high-cholesterol diet can lead to fatty plaque deposits in the macular vessels, which can hamper blood flow and increase the risk of AMD. A diet low in fat promotes good eye health. Skip foods and processed baked goods with high-fat content. In addition recent research has indicated that those consuming red meat (10 times a week or more) were at 47% higher risk for macular degeneration.
Vitamins and Supplements
The National Eye Institute’s Age-Related Eye Disease Study (AREDS) found that taking a specific high-dose formulation of antioxidants and zinc significantly reduces the risk of advanced AMD and its associated vision loss. Slowing AMD’s progression from the intermediate stage to the advanced stage will save the vision of many people.
People who should consider taking the combination of antioxidants plus zinc include those who are at high risk for developing advanced AMD. These people are defined as having either:
Intermediate AMD in one or both eyes. Intermediate AMD is defined as the presence of either many medium-sized drusen or one or more large drusen.
Advanced AMD in one eye, but not the other eye. Advanced AMD is defined as either a breakdown of light-sensitive cells and supporting tissue in the central retinal area (advanced dry form), or the development of abnormal and fragile blood vessels under the retina (wet form) that can leak fluid or bleed. Either of these forms of advanced AMD can cause vision loss. Ask you doctor if taking this special formulation is right for you and where you can obtain the specific formula in your country.[3]
Grapes May Help Prevent AMD
Can eating grapes slow or help prevent the onset of age-related macular degeneration (AMD), a debilitating condition affecting millions of elderly people worldwide? Results from a new study published in Free Radical Biology and Medicine suggest this might be the case. The antioxidant actions of grapes are believed to be responsible for these protective effects.[4]
Home Remedies and Lifestyle Changes [7]
The risk factors for macular degeneration are similar to those of heart disease and stroke.For this reason, lifestyle changes that benefit your heart may also benefit your vision. Lifestyle modifications to consider include:
Quitting smoking
Making dietary changes, such as limiting foods high in saturated fats (meat, butter, and cheese) and eating a heart-healthy diet full of whole grains, fruits, and vegetables
Maintaining weight, since obesity is also a risk factor of dry AMD
Managing blood pressure
Using sun protection, such as wearing wide-brimmed hats and sunglasses
Getting regular exercise (at least 30 minutes of physical activity every day)
As central vision declines in late-stage dry AMD, you can use low-vision tools, such as magnifying tools and handheld computers, to help with daily activities. Low-vision techniques, like using high-lumen light sources, reducing glare, and increasing contrast, can also help compensate for central vision loss.
Discussion. This systematic review and meta-analysis has shown that 8·7% of the worldwide population has age-related macular degeneration, and the projected number of people with the disease is around 196 million in 2020, increasing to 288 million in 2040.[5]
Toxoplasmosis is a parasitic disease caused by the protozoanToxoplasma gondii. The parasite infects most genera of warm-blooded animals, including humans, but the primary host is the felid (cat) family. Animals are infected by eating infected meat, by ingestion of feces of acat that has itself recently been infected, or by transmission from mother to fetus. Cats are the primary source of infection to human hosts, although contact with raw meat, especially pork, is a more significant source of human infections in some countries. Fecal contamination of hands is a significant risk factor.[1]
What is Toxoplasmosis of the eye and what causes it?
A germ called toxoplasma can cause infection within the eye. This is known as toxoplasmosis of the eye. The infection causes damage to the eye that can lead to visual impairment.
In a healthy individual, Toxoplasmosis does not produce any symptoms but in immune compromised people there may be symptoms.
Some of the symptoms of Toxoplasmosis are: [3]
Severe body pains
Lymph node swelling
Headaches
Fever
Lethargy
Many animals are infected with this germ, including cats. The germ is found in the faeces of these infected animals. A person can catch an infection if they eat food dirtied by faeces with the toxoplasma germ. Foods that can lead to an infection include some uncooked meats, unpasteurised milk and raw vegetables. The toxoplasma germ does not survive cooking or boiling.
Most adults do not know they have caught an infection. Most adults do not develop any problems from a toxoplasma infection and do not get toxoplasmosis of the eye. In fact most adults in the UK, if tested, have had a toxoplasma infection at some time in their lives but have normal eyes. eResearch by Navid Ajamin -- spring 2012
Toxoplasmosis of the Eye is mainly a problem for unborn babies
If a pregnant mother becomes infected with toxoplasma the germ can also infect the unborn child. A Toxoplasma infection in an unborn child is more serious than in an adult. The infection can cause inflammation and damage to many parts of the body. The eye is often affected (toxoplasmosis of the eye). The most common part of the eye to become affected is the retina and choroid. This is called retinochoroiditis. When the inflammation settles a scar is usually left on the retina.
In United States, pregnant females are not checked during their pregnancy for Toxoplasmosis and neither are the infants screened and without proper screening this disease is difficult to diagnose. In case if the physician suspects Toxoplasmosis, then he or she will order blood tests to look for antibodies of the parasite and if found then Toxoplasmosis is more or less confirmed. If a pregnant female is diagnosed with Toxoplasmosis, then it becomes imperative to determine whether the baby is also infected or not.
For that the following tests can be done:
Diagnose ocular toxoplasmosis
Amniocentesis: This procedure can be safely done during the second trimester. The physician removes some fluid from the fluid in the amniotic sac surrounding the fetus and investigations are carried out.
Ultrasound scan: This test cannot diagnose Toxoplasmosis, but it can definitely tell the signs of the disease such as presence of hydrocephalus in the baby. Since this test does not rule out Toxoplasmosis, hence the newborn will need blood tests within the first year of life to exclude the diagnosis of Toxoplasmosis in case if the mother was infected.[3]
How does toxoplasmosis of the eye affect the way a child sees?
Most young children will feel their vision to be 'normal' as they have never known anything else but their own visual world. At first they assume that everyone else has vision the same as their own. They do not realise that other people see things differently.
The U.S. Centers for Disease Control and Prevention (CDC) lists eating undercooked meat (especially pork, lamb and venison) and handling raw meat or the surfaces it comes into contact with as the most common forms of transmission. Contaminated drinking water is another potential source of infection, which is what happened in British Columbia, Canada, in 1995, when an outbreak was traced to a municipal water supply.
Cats, or the entire Felid family to be more accurate, are the definitive host for theT. gondii parasite. That means the parasite can only complete its full sexual life cycle in the digestive tract of a feline. (Other species that can become infected are considered “intermediate hosts” because the parasite can only undergo asexual reproduction.) The domestic cat and wild cat species become infected by consuming infected meat or water, and will then shed oocysts (the fertilized egg of the parasite) in their feces for one to three weeks. The vast majority of infected cats don’t exhibit any clinical symptoms.
In the U.S., the prevalence of cats who are actively shedding oocysts is quite low—approximately 1 percent, according to the Companion Animal Parasite Council. The oocyst shedding leads to the other mode of infection for people and other warm-blooded animals: consuming feces that contain the oocysts, such as by eating a plant with feces residue or by gardening and not washing your hands before eating.[4]
The toxoplasma germ can cause scarring of any part of the retina. But it tends to cause scarring of the central bit. If this happens then the central part of the vision will also be missing. The child will not usually notice if a part of the retina away from the centre is scarred.
Toxoplasma can affect one or both eyes. If the central bit of the retina in both eyes is scarred then the child will have blurred vision with the central part missing. The vision around the sides will still be OK. This vision is useful for getting around and not bumping into things. The child will however have difficulty reading and recognising faces. Sometimes fast to-and-fro movements of the eyes occur. This is called Nystagmus. Squint may also develop.
Toxoplasma Gondii is a unicellular parasite. This parasite is found to reproduce only in cats. When a human is infected with this parasite, it tends to form cysts almost anywhere in the entire body usually the brain or heart. Under normal circumstances, the parasite is kept quiet by the immune system of the body but in cases when the immune system is compromised like in the elderly population or in pregnant females this parasite becomes active causing potentially serious complications. A human can get infected with the parasite if he or she comes in contact with cat feces, which is infected, or if an individual has been gardening out in the yard and accidentally touches the mouth. People who eat pork, lamb etc. are more prone to get this disease. The parasite can be present in kitchen utensils which have been in contact with raw meat. Eating fruits without properly washing them is also a risk factor for getting Toxoplasmosis.
Fig. 1: Normal retina
Fig. 2: Congenital toxoplasmosis scar
Sometimes Toxoplasma can cause other eye conditions
Toxoplasma usually causes inflammation and scarring of the retina and choroid. It can however also cause other eye conditions. These include:
Clouding of the lens (cataract)
The eye can be smaller than usual (microphthalmia)
Loss of some of the communication wires from the optic nerve (optic atrophy)
Damage to the 'vision' parts of the brain (cerebral visual impairment)
Toxoplasma may cause other conditions to develop
Other conditions can also develop because of a Toxoplasma infection. These include:
Epilepsy
Difficulty with hearing
Learning difficulties
Blockage of the flow of fluid in the brain (hydrocephalus)
Fortunately most children do not develop these other problems.[2]
People at risk forocular toxoplasmosis[7]
Some people (including those with healthy immune systems) are at risk of getting ocular toxoplasmosis. Ocular toxoplasmosis causes inflammation of the retina in the back of the eye. It can lead to blindness if not treated. Symptoms include:
blurred or reduced vision
seeing floaters in your visionCan babies get toxoplasmosis from cats ?
sensitivity to light
eye redness and pain
tearing
Symptoms in babies [7]
For unborn babies, toxoplasmosis can cause a miscarriage. Babies carried to term are often born with:
low birth-weight
enlarged liver or spleen
jaundice (yellowing of the skin and eyes)
ocular toxoplasmosis
Many babies are born with no symptoms but still carry the infection. Some will develop problems years later like:
eye infections and vision loss
learning disabilities
hearing loss
Is toxoplasmosis hereditary? [8]
Toxoplasmosis is not passed from person-to-person, except in instances of mother-to-child (congenital) transmission (mother passing an infection to her baby during pregnancy or at birth) and blood transfusion or organ transplantation.
Diabetes is a disease that occurs when the pancreasdoes not secrete enough insulin or the body is unable to process it properly. Insulin is the hormone that regulates the level of sugar (glucose) in the blood. Diabetes can affect children and adults.
What causes diabetic retinopathy? [6]
Glucose, or blood sugar, is a main source of energy — yet too much circulating in the blood can be harmful to the body.
Typically, the pancreas releases the hormone insulin, which helps cells absorb glucose for energy. In the case of diabetes, though, the body doesn’t make enough insulin or doesn’t use it properly. This causes glucose to accumulate in the blood.
Consistent levels of high blood sugar can affect different parts of the body, including the eyes.
Diabetic retinopathy doesn’t only weaken or damage the blood vessels in the eye. It can also cause the development of new abnormal blood vessels in the retina.
The 4 Stages of Diabetic Retinopathy [5]
There are two types of diabetic retinopathy, which progresses in four stages.
The two types of diabetic retinopathy are nonproliferativeand proliferative.
Nonproliferative refers to the early stages of the disease, while proliferative is an advanced form of the disease.
This is the earliest stage of diabetic retinopathy, characterized by tiny swellings/bulges in the blood vessels of the retina. These areas of swelling are known as microaneurysms.
These microaneurysms can cause small amounts of fluid to leak into the retina, triggering swelling of the macula – the back of the retina. Despite this, there are usually no clear symptoms indicating there is a problem.
At this stage, the tiny blood vessels further swell up, blocking blood flow to the retina and preventing proper nourishment. This stage will only cause noticeable signs if there is a build-up of blood and other fluids in the macula, causing vision to become blurry.
Stage 3: Severe nonproliferative diabetic retinopathy
During this stage, a larger section of blood vessels in the retina becomes blocked, causing a significant decrease in blood flow to this area. The lack of blood triggers a signal to the body to start growing new blood vessels in the retina.
These new blood vessels are extremely thin and fragile and cause retinal swelling, resulting in noticeably blurry vision, dark spots and even patches of vision loss. If these vessels leak into the macula, sudden and permanent vision loss may occur. At this stage, there is a high chance of irreversible vision loss.
Stage 4: Proliferative diabetic retinopathy
At this advanced stage of the disease, new blood vessels continue to grow in the retina. These blood vessels, which are thin and weak and prone to bleeding, cause scar tissue to form inside the eye. This scar tissue can pull the retina away from the back of your eye, causing retinal detachment. A detached retina typically results in blurriness, reduced field of vision, and even permanent blindness.
How does diabetes affect the retina?
Patients with diabetes are more likely to develop eye problems such as cataracts and glaucoma, but the effect of the disease on the retina is the main threat to vision. Most patients develop diabetic changes in the retina after approximately 20 years.The effect of diabetes on the eye is called diabetic retinopathy. eResearch by Navid Ajamin -- spring 2012
Over time, diabetes affects the circulatory system of the retina. The earliest phase of the disease is known as background diabetic retinopathy. In this phase, the arteries in the retina become weakened and leak, forming small, dot-like hemorrhages. These leaking vessels often lead to swelling or edema in the retina and decreased vision.
The next stage is known as proliferative diabetic retinopathy. In this stage, circulation problems cause areas of the retina to become oxygen-deprived or ischemic. New, fragile, vessels develop as the circulatory system attempts to maintain adequate oxygen levels within the retina. This is called neovascularization. Unfortunately, these delicate vessels hemorrhage easily. Blood may leak into the retina and vitreous, causing spots or floaters, along with decreased vision.
In the later phases of the disease, continued abnormal vessel growth and scar tissue may cause serious problems such as retinal detachment and glaucoma.
Diabetic retinopathy (DR) is a common complication of diabetes mellitus and is a major cause of vision loss in middle-aged and elderly people. One-third of people with diabetes have DR. Severe stages of DR include proliferative DR, caused by the abnormal growth of new retinal blood vessels, and diabetic macular oedema, in which there is exudation and oedema in the central part of the retina. DR is strongly associated with a prolonged duration of diabetes, hyperglycaemia and hypertension. It is traditionally regarded as a microvascular disease, but retinal neurodegeneration is also involved. Complex interrelated pathophysiological mechanisms triggered by hyperglycaemia underlie the development of DR. These mechanisms include genetic and epigenetic factors, increased production of free radicals, advanced glycosylation end products, inflammatory factors and vascular endothelial growth factor (VEGF). Optimal control of blood glucose and blood pressure in individuals with diabetes remains the cornerstone for preventing the development and arresting the progression of DR. Anti-VEGF therapy is currently indicated for diabetic macular oedema associated with vision loss, whereas laser photocoagulation prevents severe vision loss in eyes with proliferative DR. These measures, together with increasing public awareness and access to regular screening for DR with retinal photography, and the development of new treatments to address early disease stages, will lead to better outcomes and prevent blindness for patients with DR.[4]
SIGNS AND SYMPTOMS
The affect of diabetic retinopathy on vision varies widely, depending on the stage of the disease. Some common symptoms of diabetic retinopathy are listed below, however, diabetes may cause other eye symptoms.
Blurred vision (this is often linked to blood sugar levels)
Floaters and flashes
Sudden loss of vision [1]
Diabetic retinopathy can be divided into non-proliferative and proliferative diseases.
Non-proliferative disease:Tiny blood vessels in the retina are damaged by diabetes that begin to leak and bleed. This leakage of fluid will cause the macula to swell and vision to be lost.
Proliferative disease: In this advanced stage of diabetic retinopathy, abnormal and fragile blood vessels grow along the retina and in the vitreous. Without timely treatment, these new vessels bleed causing scar tissue to grow and can lead to blindness.[3]
DETECTION AND DIAGNOSIS
Diabetic patients require routine eye examinations so related eye problems can be detected and treated as early as possible. Most diabetic patients are frequently examined by an internist or endocrinologist who in turn work closely with the ophthalmologist.
The diagnosis of diabetic retinopathy is made following a detailed examination of the retina with an ophthalmoscope. Most patients with diabetic retinopathy are referred to vitreo-retinal surgeons who specialize in treating this disease.[1]
TREATMENT
Treatment for diabetic retinopathy depends on the stage of the disease and is directed at trying to slow or stop the progression of the disease.
In the early stages of Non-proliferative Diabetic Retinopathy, treatment other than regular monitoring may not be required. Following your doctor's advice for diet and exercise and keeping blood sugar levels well-controlled can help control the progression of the disease.
Some bleeding into the vitreous gel may clear up on its own. However, if significant amounts of blood leak into the vitreous fluid in the eye, it will cloud vision and can prevent laser photocoagulation from being used. A surgical procedure called a vitrectomy may be used to remove the blood-filled vitreous and replace it with a clearfluid to maintain the normal shape and health of the eye.
Persons with diabetic retinopathy can suffer significant vision loss. Special low vision devices such as telescopic and microscopic lenses, hand and stand magnifiers, and video magnification systems can be prescribed to make the most of remaining vision.[2]
PREVENTION
Researchers have found that diabetic patients who are able to maintain appropriate blood sugar levelshave fewer eye problems than those with poor control. Diet and exercise play important roles in the overall health of those with diabetes.
Diabetics can also greatly reduce the possibilities of eye complications by scheduling routine examinations with an ophthalmologist.
Many problems can be treated with much greater success when caught early.[1]
Retinitis pigmentosa (RP) is a rare, hereditary disease that causes the rod photoreceptors in the retina to gradually degenerate. The rods are located in the periphery of the retina and are responsible for peripheral and night vision. Cones, another type of photoreceptor, are densely concentrated in the macula. The cones are responsible for central visual acuity and color vision.
Rather than being considered a single disease, retinitis pigmentosa instead is viewed as a group of diseases affecting how light-sensitive cells in the back of the eye function. Not much is known about what causes retinitis pigmentosa, except that the disease is inherited.
The eye condition is associated with at least 32 different genes, which control traits that are passed along in a number of different ways. At times, the genetic trait is dominant and likely to be passed along to a child when a parent has RP. At other times, the trait for retinitis pigmentosa is recessive and may be present for many generations before it appears in a family member.
This means that, even if your mother and father don't have retinitis pigmentosa, you can still have the eye disease when at least one parent carries an altered gene associated with the trait. In fact, about 1 percent of the population can be considered carriers of genetic tendencies for retinitis pigmentosa.
Retinitis pigmentosa occurs in about 1 of every 4,000 people in the United States. When the trait is dominant, it is more likely to show up when people are in their 40s. When the trait is recessive, it tends to first appear when people are in their 20s.
The disease may be X-linked (passed from a mother to her son), autosomal recessive (genes required from both parents) or autosomal dominant (gene required from one parent) trait. Since it is often a sex-linked disease, retinitis pigmentosa affects males more than females.
People with RP usually first notice difficulty seeing in dim lighting and gradually lose peripheral vision. The course of RP varies. For some, the affect on vision may be mild. Others experience a progression of the disease that leads to blindness.
In many cases, RP is diagnosed during childhood when the symptoms begin to become apparent. However, depending on the progression of the disease, it may not be detected until later in life.
Rod and cone photoreceptor cell death in retinitis pigmentosa. Rod cell death due to the deleterious genetic mutations is associated with apoptosis, which involves the activation of caspase-independent pathways including poly-ADP-ribose-polymerase (PARP), calpain and histone deacetylase (HDAC). Cone cell death is induced by the microenviromental changes subsequent to rod degeneration, such as oxidation, inflammation and loss of trophic factors. Dying cones show different morphological features from rod cells, such as necrotic cytoplasmic swelling (asterisk), and is partly mediated through the activation of RIP kinase (RIPK). Electron microscopy images were reproduced with permissions from Murakami et al.5 mToR, mammalian target of rapamycin; RdCVF, rod-derived cone viability factor; TNF-α, tumor necrosis factor-α
SIGNS AND SYMPTOMS
Some of the most common symptoms of retinitis pigmentosa include:
Decreased vision at night or in low light
Loss of side (peripheral) vision, which may cause the person to bump into tables, furniture, or doorways. It may not be noticed by the person with retinitis pigmentosa, but may be apparent to others.
Loss of central vision (in advanced cases)
Other indicators of retinitis pigmentosa are your family history (especially the possibility of retinitis pigmentosa appearing in other family members) and expressed visual concerns or complaints, such as not being able to see well at night or in low light conditions.
Difficulty seeing dim lighting
Tendency to trip easily or bump into objects when in poor lighting
Gradual loss of peripheral vision
Glare
Loss of contrast sensitivity
Eye fatigue (from straining to see)
The initial retinal degenerative symptoms of retinitis pigmentosa are characterized by decreased night vision (nyctalopia) and the loss of the mid-peripheral visual field. The rod photoreceptor cells, which are responsible for low-light vision and are orientated in the retinal periphery, are the retinal processes affected first during non-syndromic forms of this disease.Visual decline progresses relatively quickly to the far peripheral field, eventually extending into the central visual field as tunnel vision increases. Visual acuity and color vision can become compromised due to accompanying abnormalities in the cone photoreceptor cells, which are responsible for color vision, visual acuity, and sight in the central visual field.The progression of disease symptoms occurs in a symmetrical manner, with both the left and right eyes experiencing symptoms at a similar rate.
A variety of indirect symptoms characterize retinitis pigmentosa along with the direct effects of the initial rod photoreceptor degeneration and later cone photoreceptor decline. Phenomena such as photophobia, which describes the event in which light is perceived as an intense glare, and photopsia, the presence of blinking, swirling or shimmering lights within the visual field, often manifest during the later stages of RP. Findings related to RP have often been characterized in the fundus of the eye as the "ophthalamic triad".
This includes the development of (1) a mottled appearance of the retinal pigment epithelium (RPE) caused by bony spicule formation, (2) a waxy appearance of the optic nerve, and (3) the attenuation of blood vessels in the retina.
Non-syndromic RP usually presents a variety of the following symptoms:
Night blindness
Tunnel vision (due to loss of peripheral vision)
Latticework vision
Photopsia (blinking/swirling/shimmering lights)
Photophobia (aversion to bright lights)
Development of bone spicules in the fundus
Slow adjustment from dark to light environments and vice versa
Blurring of vision
Poor color separation
Loss of central vision
Eventual blindness
DETECTION AND DIAGNOSIS
It is a painless test. The ERG, in conjunction with the visual field exam, will usually make the diagnosis. The ERG will also determine if there is any involvement of the central retina and visual field. Periodic follow-up ERG examinations are necessary to follow and track the progression of your retinitis pigmentosa.
Retinitis pigmentosa is usually diagnosed before adulthood. It is often discovered when the patient complains of difficultly with night vision. The doctor diagnoses RP by examining the retina with an ophthalmoscope. The classic sign of RP is clumps of pigment in the peripheral retinal called "bone-spicules." A test called electroretinography (ERG) may also be ordered to study the eye's response to light stimuli. The test gives the doctor information about the function of the rods and cones in the retina. eResearch by Navid Ajamin -- spring 2012
Color fundus photograph of a patient with typical RP. There is peripheral bone spicule deposition encroaching into the macula, optic nerve pallor, and prominent vascular attenuation. The central retina and RPE are preserved (“central island”).
OCT B-scan corresponding to the Color fundus photograph . There is significant thinning of the outer retinal layers and dropout of the RPE involving the edges of the macula. However, the central fovea is spared with normal retinal architecture.
Retinitis pigmentosa (RP) refers to a heterogeneous group of inherited disorders that are characterized by loss of retinal cell function, preferentially in the peripheral retina. RP can have varying severity, age of onset, mode of inheritance, and systemic associations. RP may be inherited in an autosomal dominant, autosomal recessive, or X-linked recessive fashion. The X-linked form of the disease is typically the most severe. The disease is often secondary to mutations in the rhodopsin gene, though some forms have been linked to mutations in the RDS gene (Anasagasti et al., 2012). Generally, RP is characterized by a slowly progressive loss of night vision (nyctalopia) along with contraction of the visual field. In later stages of the disease central acuity is affected, which may cause profound vision loss. Typical fundus abnormalities include waxy pallor of the optic nerve, a tapetal-like reflex resulting from changes in the retinal pigment epithelium (RPE), narrowing of the peripheral retinal vasculature, and bone-spicule changes in the mid-peripheral retina. Definitive diagnosis requires electrophysiologic testing. Computed tomography is useful to aid in the initial diagnosis and detecting associated macular abnormalities such as cystoid macular edema.
Genetic Testing
Recently, testing for genetic defects is being done to clarify the loss in more detail and to find a treatment.
It is important to make a diagnosis so that the patient and family can be counseled as to the status of the disease, when driving might have to be discontinued, and what low vision interventions and low vision devices (in the case of more advanced disease) might be available to allow maximum use of the patient's visual potential.
TREATMENT
A group of eye problems that affect the retina, retinitis pigmentosa (RP) is a rare group of hereditary diseases that causes the photoreceptors in the retina to gradually degenerate.
People with retinitis pigmentosa lose their vision slowly over time, as it changes how the retina responds to light, making it hard to see.
The type and speed of vision loss from retinitis pigmentosa varies from person to person – it depends on their form of the condition.
There is currently no standard treatment or therapy for retinitis pigmentosa; however, scientists have isolated several genes responsible for the disease. Once RP is discovered, patients and their families are encouraged to seek genetic counseling.
There are few treatment options such as light avoidance and/or the use of low-vision aids to slow down the progression of RP. Some practitioners also consider vitamin A as a possible treatment option to slow down the progression of RP. Research suggests taking high doses of vitamin A (15,000 IU/day) may slow progression a little in some people, but the results are not strong. Taking too much vitamin A can be toxic and the effects of vitamin A on the disease is relatively weak. More research must be conducted before this is a widely accepted form of therapy.
Research is also being conducted in areas such as gene therapy research, transplant research, and retinal prosthesis. Since RP is usually the result of a defective gene, gene therapy has become a widely explored area for future research. The goal of such research would be to discover ways healthy genes can be inserted into the retina. Attempts at transplanting healthy retinal cells into sick retinas are being made experimentally and have not yet been considered as clinically safe and successful. Retinal prosthesis is also an important area of exploration because the prosthesis, a man-made device intended to replace a damaged body part, can be designed to take over the function of the lost photoreceptors by electrically stimulating the remaining healthy cells of the retina.Through electrical stimulation, the activated ganglion cells can provide a visual signal to the brain. The visual scene captured by a camera is transmitted via electromagnetic radiation to a small decoder chip located on the retinal surface. Data and power are then sent to a set of electrodes connected to the decoder. Electrical current passing from individual electrodes stimulate cells in the appropriate areas of the retina corresponding to the features in the visual scene.
Visual field examination: Left: normal findings, right: tubular visual field loss in retinitis pigmentosa
لکهٔ زرد یا ماکولا (به انگلیسی: Macula) بخشی از شبکیه است که بیشترین حساسیت به نور را دارد و موجب دید مستقیم و واضح میشود. لکه زرد برای کارهای دقیق مثل خواندن و رانندگی لازم است.
این لکه با شکل بیضوی حاوی رنگدانههای زرد و در نزدیکی مرکزشبکیه است. فووه آ (fovea) که بیشترین تراکم سلولهای مخروطی چشم را داراست در ماکولا قرار دارد. سلولهای مخروطی گونهای از سلولهای گیرندهٔ نور هستند که به مغزتوانایی دیدن رنگها و جزئیات ظریف اشیا را میدهند و بیشتر در نور قوی تحریک میشوند. بنابراین، این بخش که در انتهای چشم و در راستای مردمک قرار دارد، در دقت و تیزبینی چشم نقش دارد. قطر لکهٔ زرد حدود ۲ میلیمتر است.[1]
یكی از مهمترین بیماریهای چشم، استحاله یا تخریب لكه زرد است كه پزشكان به آن «دژنراسیون ماكولا» میگویند. تخریب لكه زرد، شایعترین علت كاهش بینایی ناشی ازبالا رفتن سن است. به عبارت دیگر، تخریب یا استحاله ماكولا، علت شایع افت دید در افراد بالای 55 سال است. از آنجایی كه این بیماری فقط دید مركزی را مختل میكند، بهندرت باعث نابینایی فرد میشود؛ با این حال میتواند خواندن، رانندگیكردن و انجام سایر فعالیتهای روزمرهای كه نیاز به دید مركزی و دقیق دارند را بسیار مشكل یا غیرممكن كند.
تباهی لکه زرد میتواند سبب کاهش دید تدریجی یا ناگهانی شود. اگر خطوط مستقیم را موجدار میبینید، دیدتان تار است، یا لکههای تیره در مرکز دید خود میبینید احتمال دارد که دچار علائم اولیه دژنراسیون ماکولا شده باشید. در بسیاری موارد قبل از اینکه بیمار دچار علائم شود چشم پزشک علائم اولیه بیماری را در معاینه تشخیص میدهد. این کار معمولاً از طریق تست میدان بینایی صورت میگیرد. در دژنرسانس ماکولا دید مرکزی مختل شده و بیمار در مرکز دید خود لکهای سیاه میبیند.[4]
دژنراسیون ماكولا بر دو نوع است: خشك (Dry) و تَر (Wet). نوع خشك شایعتر بوده و حدود ۹۰% بیماران به این نوع مبتلا می شوند. نوع تَر معمولا با كاهش دید شدیدتر و جدی تری همراه است.
زنان بیشتر به این بیماری مبتلا می شوند. اكثر موارد این بیماری با افزایش سن بوجود می آیند. این بیماری می تواند عارضه بعضی داروها نیز باشد. همچنین به نظر می رسد ارث نیز در ابتلا به این بیماری نقش داشته باشد.
علت دقیق این بیماری هنوز شناخته نشده است. نوع خشك ممكن است بر اثر پیر و نازك شدن بافت ماكولا، رسوب رنگدانه ها در ماكولا، و یا تركیبی از این دو ایجاد شود. در نوع تَر عروق خونی جدید در زیر شبكیه رشد كرده و خون و مایع از آنها نشت می كند. این نشت سبب مرگ سلولهای شبكیه شده و باعث ایجاد نقاط كور در دید مركزی می شود. عواملی كه شانس ابتلا به بیماری را افزایش می دهد عبارتند از: سابقه خانوادگی، مصرف سیگار، فشار خون بالا، دوربینی و چاقی.
دانشمندان در تحقيقاتي جديد اظهار داشته اند سیگاریهاچهار برابر بیشتر از کسانی که سیگار نمی کشند در معرض نابینایی حاصل از تخریب لکه زرد چشم قرار دارند.
تحقیقات جدید نشان می دهد: بیش از ۲۵ درصد تخریب لکه زرد و اختلالات بینایی به علت کشیدن سیگار در زمان حال یا گذشته است و درمان موثری برای آن وجود ندارد.
افراد سیگاری در مقابله با افرادی که هرگز سیگار نکشیده اند، چهار برابر خطر ابتلا به عارضه تنفسی دارند و از دیدگاه زیست شناختی، شبکیه به علت تخریب اکسیداتیو حاصل از کشیدن سیگار، صدمه می بیند. eResearch by Navid Ajamin -- autumn 2011
این تخریب توسط رادیکال های آزاد که مولکول های ناپایدار سمی هستند، صورت می گیرد و به حدی شدید است که عوامل حفاظتی مانند وجود مواد ضد اکسید در رژیم غذایی در بهبود آن موثر نیست.
همچنین تخریب لکه زرد باعث از بین رفتن دید مرکزی شده و منجر به ناتوانی در به کارگیری شبکیه جهت فعالیت هایی مانند خواندن، دوختن و حتی رانندگی می شود.
What is the macula?
The macula is part of the retina at the back of the eye. It is only about 5mm across but is responsible for all of our central vision, most of our colour vision and the fine detail of what we see.
The macula has a very high concentration of photoreceptor cells that detect light and send signals to the brain, which interprets them as images. The rest of the retina processes our peripheral (side) vision. Macular disease causes loss of central vision.[7]
Macular degenerations are retinal diseases of genetic origin that cause an early degeneration of the macula. It affects adults, young people or even children, it all depends on the severity of the damage caused by this genetic anomaly.
The macula deteriorates and collapses affecting vision and causing a loss of vision that may be important and reach legal blindness.
It is a hereditary disease and, therefore, different from age-related macular degeneration (AMD), which is caused by the aging of the body.
This disorder can manifest itself in various forms such as Stargardt’s disease, Best’s vitelliform macular dystrophy and juvenile retinoschisis.
Age-Related Macular Degeneration
What is juvenile macular degeneration?
This disease consists of the deterioration of the macula of the eye. The macula is the part of the retina responsible for the central vision and allows us to see fine and small details clearly.
The macula is much more sensitive to detail than the rest of the retina (peripheral retina, allows lateral vision) and, therefore, if it is affected, the quality of vision is reduced.
When the macula is affected, the central vision is lost and causes unfocused vision and lack of sharpness.
Who can develop this disorder?
It is a hereditary disease, so it is transmitted from parents to children.
In the case of Stargardt’s disease, being recessive, it is only inherited if the two parents are affected by the gene.
In the case of Best’s vitelliform macular dystrophy, it can be suffered even if only one of the parents is affected.
Juvenile retinoschisis is a disease linked to the X chromosome and, therefore, affects males, but it is transmitted from mother to child.
What are the symptoms of juvenile macular degeneration?
Some of the symptoms of juvenile macular degeneration can be:
Problems in the central vision that make it difficult to perform activities such as reading small print or traffic signs or threading a needle.
Blurred, distorted vision with dark areas.
Photophobia (sensitivity to light)
Display of black and gray spots.
Yellowish flecks around the macula.
Impairment of color perception.
Symptoms appear during childhood and / or adolescence and can affect one or both eyes. Lateral vision is not usually affected.
In some cases, patients can maintain useful vision for decades (Best’s vitelliform macular dystrophy) and, in other cases, vision can be lost to legal blindness (Stargardt’s disease).
How is this disorder diagnosed?
Normally, in Stargardt’s disease small yellow spots are visualized in the macula that may extend outwards.
On the other hand, patients with Best’s vitelliform macular dystrophy have a yellowish cyst under the macula, like an egg yolk that, over time, breaks down and looks like a scrambled egg.
Patients with juvenile retinoschisis have a retina that separates into two layers, with spaces between the layers that can be filled with cysts and blood vessels, which can break and cause hemorrhages. This tearing of the layers of the retina can cause a retinal detachment.
What tests are done to diagnose macular degeneration?
The ophthalmologist will perform an ocular dilatation test in order to observe the retina and be able to confirm that there are specific signs related to this disorder.
The ophthalmologist can also perform a fluorescein angiogram to confirm the diagnosis and, if needed, recommend an ERG (electroretinography) to measure the electrical activity of the retina.
More recent tests such as optical coherence tomography (OCT) and autofluorescent retinography provide complementary information of great importance, especially to objectify the progression of the disease.[6]
Age-related macular degeneration in an 82-year-old white male. Colour photographs of the right and left eyes (a, b) show numerous drusen in the posterior pole and fundus tessellation in the macula. Spectral domain optical coherence tomography of the right and left eyes (c, d) shows bilateral drusen. In the left eye (d), there is a large irregular pigment epithelial detachment with hyperreflective contents and adjacent subretinal fluid, consistent with type 1 neovascularization. The choroid is relatively thin in both eyes. Fundus autofluorescence of the right and left eyes (e, f ). There is a hypoautofluorescent geographic focus at the fovea of the left eye (f ) with a curvilinear hyperautofluorescent zone inferior to the fovea, hinting at a legacy of chronic subretinal fluid. Late transit and recirculation fluorescein angiography of the left eye (g) shows irregular hyperfluorescence at the inferior border of the fovea with late, poorly defined staining. There is also extensive staining of drusen. Indocyanine green angiography of the right eye (g) shows no evidence of neovascularization. Indocyanine green angiography of the left eye (h) shows a hyperfluorescent 'plaque' indicating the full extent of the type 1 neovascular lesion.[5]
Treatment for macular degeneration
To this day, there is no treatment to prevent or stop this disorder.
It is important to wear sunglasses with ultraviolet protection, it is recommended to avoid supplements with vitamin A, and it is advisable to perform mobility exercises for patients to adapt to vision loss.[6]
پژوهش ها نشان می دهد: وقتی سیگار ترک شود چشم ها در برابر صدمات بیشتر مصون می مانند و خطر ابتلا به این عارضه در این افراد نسبت به کسانی که تا به حال سیگار نکشیده اند کمی افزایش می یابد.
بر اساس نتیجه این بررسی افراد سیگاری با ترک سیگار می توانند احتمال از بین رفتن سلول های شبکیه چشم خود را کاهش دهند.
بر این اساس ، احتمال ابتلا به این عارضه در افرادی که ۲۰ سال پیش سیگار را ترک کرده اند تا حد یک فرد غیرسیگاری کاهش می یابد.
عارضه تحلیل لکه زرد چشم ، شایع ترین علت نابینایی افراد سالمند است.
ماکولا یا لکه زرد در مرکز شبکیه قرار دارد. شبکیه هم، لایه حساس به نور است که در قسمت خلفی کره چشم قرار دارد. نور روی ماکولا متمرکز میشود. در ماکولا میلیونها سلول مخصوص بینایی وجود دارد.
ماکولا یا لکه زرد نور را دریافت و به علائم عصبی تبدیل کرده، به مغز منتقل میکند. این روند دید مرکزی نامیده میشود.
در واقع دید مرکزی، توانایی رانندگی کردن، خواندن و انجام فعالیتهایی که نیاز به دید مستقیم، دقیق و ظریف دارد را فراهم میآورد. اگر ماکولا صدمه ببیند، قسمت مرکزی تصویر دیده شده تار میشود و تصویر در اطراف منطقه تار شده وضوح بیشتری دارد.
پس اهمیت لکه زرد در این است که در قسمتی از شبکیه که نزدیک عصب بینایی است، سلولهای اصلی بینایی که مخصوص دید در روز، دید دقیق و دید رنگی هستند، تجمع پیدا کردهاند. در واقع انسان به وسیله لکه زرد بهترین و دقیقترین دید را به دست میآورد.[2]
روش های درمان دژنراسیون ماکولا
این بیماری درمان قطعی ندارد ولی درمان هایی برای جلوگیری از پیشرفت بیمار و یا حتی بهبود دید وجود دارد. درمان استاندارد این بیماری دربرگیرنده تزریق یک ضد فاکتور رشد اندوتلیوم عروقی است که از پیشروی بیشتر رگهای خونی جلوگیری می کند.
ویتامین ها
در حال حاضر به نظر می رسد بهترین راه برای محافظت از چشم ها از تشدید زودرس ماکولا، داشتن یک رژیم سالم، استفاده از عینک های آفتابی است که چشم شما را از اشعه های مضر UV و اشعه ماوراء بنفش (HEV) محافظت می کند.
ویتامین های آنتی اکسیدان نظیر ویتامین A و ویتامین های C و E ممکن است ماکولا را در برابر تخریب محافظت کنند. مشخص شده است که مصرف ویتامینهای C و E، ویتامین A و روی، خطر پیشرفت بیماری را در بعضی بیماران تا ۲۸٪ کاهش میدهد. از اینرو به بیماران در خطر ابتلا به نوع پیشرفته توصیه می شود آنتیاکسیدان و روی مصرف کنند.
جراحی کاشت لنز تلسکوپی
برای درمان دژنراسیون ماکولا خشک پیشرفته در هر دو چشم، یک گزینه برای بهبود دید ممکن است عمل جراحی کاشت لنز تلسکوپی در یک چشم باشد. لنز تلسکوپی، که شبیه یک لوله پلاستیکی کوچک است، با لنزهای بزرگ برای میدان دید مجهز شده است. ایمپلنت لنز تلسکوپی ممکن است بینایی دور و نزدیک را بهبود بخشد،و همچنین می تواندبرای کمک در شناسایی نشانه های خیابانی مفید باشد.
درمان دارویی با ویزودین (Visudyne)
ویزودین اولین دارویی است که برای نوع تَر بکار می رود. در این روش درمانی، دارو به دست بیمار تزریق شده و سپس با استفاده از یک لیزر غیر حرارتی فعال می شود. فعال شدن دارو سبب ایجاد واکنشی شیمیایی می شود که عروق خونی غیر طبیعی را از بین می برد. از هر 6 بیمار درمان شده یک نفر دید بهتری پیدا می کند و این دو برابر بیمارانی است که از این دارو استفاده نمی کنند.
فیلتراسیون خونی(Blood Filtration)
در این روش که حدود 2 دهه پیش توسط ژاپنیها ابداع شد جریان متفاوت خون در غشاء سبب کاهش مقدار بعضی از پروتئینها و اسیدهای چرب که مقدارشان زیاد است و ممکن است مضر باشند، میشود. این تکنیک در بیماریهای مختلفی بکار گرفته شده است ولی نوع جدیدی از آن بنام رئوفرزیس (Rheopheresis) برای درمان نوع خشک AMD تست شده است. رئوفرزیس هنوز توسط سازمان غذا و داروی آمریکا (FDA) تأیید نشده است ولی بصورت تجارتی در کانادا و اروپا در دسترس است.[3]
فوتوکوآگولاسیون با لیزر (Laser Photocoagulation) با تخریب و عایق بندی عروق خونی جدید و جلوگیری از نشت خون و مایع باعث بهبود بیماران مبتلا به نوع تَر میشود. در این روش جای لیزر مانند زخمی بر روی شبکیه باقی میماند و باعث به وجود آمدن نقاط کور در دید بیمار میشود.[4]
مگسپران در حقیقت سایه کدورتهای موجود در مایع زجاجیهVitreous humor داخل چشم است که به صورت سایه های تیره دیده میشود. علت آن می تواند ناشی از ضخیم شدن رشتههای زجاجیه، جمع شدن سلولهای التهابی و یا خونریزی در داخل چشم باشد.
هنگام خیره شدن به یک زمینه روشن و صاف (مثل آسمان آبی یا دیوار سفید) این پدیده به صورت ذرات کوچک غبار مانندی جلوی چشم ظاهر و حرکت می کند. با حرکت چشم این ذرات نیز حرکت می کنند.
علت مگسپران چیست؟
مگسپران در بین تمام سنین شایع است. با افزایش سن شیوع آن زیاد می شود، به طوریکه بیش از ۷۰- ۶۰% افراد بالای ۶۰ سال مگسپران را تجربه کردهاند. رشتههای موجود در مایع زجاجیه چشم در کودکان و افراد جوان معمولاً بسیار ظریف است و دیده نمیشود اما با بالا رفتن سن این رشتهها ضخیمتر میشوند و در بعضی جاها به هم میچسبند و باعث ایجاد کدورت میشوند که سایه این کدورت بر روی شبکیه به صورت مگسپران احساس میشود. در بسیاری از افراد مسن بخشی از رشتههای محیطی زجاجیه که به شبکیه متصل بوده و از جای خود کنده میشود و به داخل بخشهای مرکزی زجاجیه میافتد. این حالت که آن را (جداشدگی خلفی زجاجیه) مینامندکه شایعترین علت ایجاد مگسپران است. گاهی اوقات هم وجود التهاب داخل چشمی (یووئیت) سبب تجمع سلولهای التهابی در زجاجیه میشود که باعث ایجاد مگسپران میشود. یک علت دیگر مگسپران وجود خونریزی در داخل زجاجیه است؛ مثلاً در افراد مبتلا به دیابت ممکن است خونریزی خفیف چشمی ابتدا به صورت یک مگسپران دیده شود.
جرقه چیست؟ به معنای دیدن یک نور در میدان بینایی بدون وجود حقیقی یک محرک نوری است. در چشم پزشکی جرقه به معنای احساس وجود نور در میدان بینایی است وقتی که در حقیقت محرک نوری وجود ندارد. می تواند به صورت خطوط درخشان یا اجسام ریز درخشنده به نظر برسد. جرقه ممکن است فقط در یک نقطه خاص و یا به صورت نقاط ریز متعدد در بخشی از میدان بینایی درآید. احساس دیدن جرقه معولاً فقط چند ثانیه طول میکشد اما غالباً تکرار می شود. معمولاً در محیطهای تاریک جرقه ها بیشتر تظاهر میکنند. به علاوه حرکات ناگهانی سر یا چشمها ممکن است باعث دیدن جرقه شود.
Floater
چگونه جرقه ایجاد می شود؟ چون پاسخ سلول های شبکیه به هر نوع محرکی بصورت درک نور می باشد، هر عامل تحریک کننده از جمله اثر مایع چسبنده زجاجیه روی شبکیه می تواند باعث جرقه شود. به همین علت وقتی شبکیه تحت کشش قرار گیرد جرقههای نوری دیده میشود.
اهمیت بررسی مگس پران و جرقه چیست؟ گاهی اوقات در حین جدا شدن زجاجیه بخشی از شبکیه نیز همراه با آن کنده میشود و باعث ایجاد سوراخ یا پارگی در پرده شبکیه میشود که می تواند سبب جدا شدن پرده شبکیه و مشکلات شدید بینایی شود. پس هر نوع مگس پران و یا جرقه جدید می بایست تحت بررسی قرار گیرد. برای انجام معاینه ابتدا مردمک با استفاده از قطرههای مخصوص باز میشود و سپس معاینه انجام میشود. در صورتی که در معاینه هیچ مشکلی به جزء (جداشدگی زجاجیه خلفی) وجود نداشته باشد و شبکیه سالم باشد معمولا خطری وجود ندارد و اقدام خاصی لازم نیست اما در مواردی که آسیبی به پرده شبکیه وارد شده باشد یا خونریزی یا التهاب داخل چشمی وجود داشته باشد باید درمان انجام شود. گاها نیاز به تکرار این معاینه در فواصل زمانی مشخص است.
درمانجرقه و مگس پران چیست؟ مگسپران معمولاً علت خطرناکی ندارد و نیازی به درمان ندارد. در اکثر موارد پس از چند هفته تا چند ماه مگس پران به تدریج کوچک می شود و فرد نیز عادت می کند که آن را ندیده بگیرد. اما در مواردی که مگس پران با سوراخ یا پارگی پرده شبکیه همراه باشد ممکن است نیاز به اقدامات درمانی مثل لیزر یا عمل جراحی برای جلوگیری از پارگی پرده شبکیه وجود داشته باشد. جرقه نیز در صورتی که علت خطرناکی نداشته باشد پس از چند روز تا چند هفته برطرف میشود و نیاز به درمان ندارد.
What Are Floaters?
As the name says, floater are structures that are floating. They are clumps of different size, shape, consistency of collagen fiber (primary floaters) or cells(secondary floaters) that develop inside the vitreous and moves with the movements of the eye.
The primary floaters are caused by the normal aging process of the vitreous and the secondary floaters as a result from other diseases (for example diabetes) or conditions (inflamation).
The shadow that these floaters cast on the retina is what we perceive like dots, lines, circles, clouds or cobwebs.
سردرد و جرقه افرادی که میگرن دارند اغلب نوع دیگری از جرقه را تجربه میکنند. این جرقهها به صورت خطوط زیگزاگی لرزان یا نقاط بزرگ شونده دیده میشود. معمولاً این جرقهها ابتدا در وسط میدان بینایی ظاهر میگردد (یعنی روبروی فرد دیده میشود) و در عرض ۱۵ تا ۲۰ دقیقه به تدریج به کنارههای میدان بینایی کشیده شده، کمکم محو میگردد. پس از آن سر درد شروع میشود که معمولاً یک طرفه و ضرباندار است. البته در بعضی از افراد فقط جرقه تظاهر میکند و سردرد اتفاق نمیافتد. این حالت را “میگرن چشمی” میگویند. یک نکته مهم آن است که جرقه ناشی از میگرن همزمان در هر دو چشم دیده میشود اما جرقه ناشی از مشکلات چشمی فقط در چشم مبتلا تظاهر میکند.ضربه ناگهانی به سر علت دیگر جرقه است.
What is Posterior Vitreous Detachment(Floaters & Flashes)?
The inside cavity of the eye is filled with a gel-like material called vitreous. When people are young, this material is dense, like jelly. As part of the aging process, the gel begins to liquefy and become more like water. As this happens, the vitreous can shrink and pull away from the retina, the tissue that lines the inner surface of the eye. When the vitreous separates from the retina, this is called a posterior vitreous detachment. In addition to aging, a posterior vitreous detachment is especially common in people who have had cataract surgery or are nearsighted.
What are the symptoms of a Posterior Vitreous Detachment?
The most common symptoms are floaters and flashes. Floaters are small clumps of vitreous gel and collagen fibrils that float around inside the eye. Floaters can look like dots, circles, line, or cobwebs, and they move when the eye moves. Sometimes, when the vitreous pulls away from the retina, it causes a small amount of bleeding into the eye, and this can cause numerous, string-like floaters. People notice floaters more often when they are in bright light, such as on a sunny day, or in a bright room with white walls. Most people get accustomed to their floaters and are no longer bothered by them. Over time, the floaters will thin and move away from the central vision. eResearch by Navid Ajamin -- spring 2011
Flashes of light, or lightening streaks, can be seen when the vitreous separates from the retina. During this process, the vitreous pulls on the retina which causes the appearance of flashing lights (the retina has no pain sensors, so traction on the retina is represented by flashes of light). Usually, the process of a posterior vitreous detachment happens over the course of several weeks, and flashes of light can be seen during this period of time.
Is a Posterior Vitreous Detachment serious?
Usually, this is not a serious problem. However, when the vitreous is pulled away from the retina, it sometimes creates a hole or tear in the retina. A retinal hole or retinal tear can lead to a retinal detachment, which is a serious problem.
When is it necessary to see a Retina Specialist if you have floaters or flashes?
Without an examination by an eye doctor, there is no way for a patient to determine if floaters or flashes are serious. If you are having new onset floaters or flashes, or a significant increase or change of these symptoms, you should be examined by a retina specialist as soon as possible. It is necessary to have a complete, dilated eye exam with scleral depression to check for retinal holes, retinal tears, or a retinal detachment.
Causes of Eye Floaters
Eye floaters, myodesopsias or muscae volitantes
Eye floaters are naturally occurring and are often a product of aging. As we get older, the proteins in our eyes break down and fibres within the vitreous become more visible, and drift through the eye’s fluid. When eye floaters are occasionally present and seem to be consistent in pattern, they can be normal.
Some people may be born with proteins or fibrous particles in the eye’s vitreous. These specks can remain in the fluid as the eye grows. Sometimes eye floaters can be confused with particles trapped under a contact lens. Other common reasons for eye floaters include:
Being over the age of 50
Nearsightedness (myopia)
Diabetic retinopathy
Eye inflammation
Previous eye trauma
Previous eye surgery
When should I worry about eye floaters?
Symptoms that should be seen by a doctor include light flashes in one or both eyes, a dark shadow or curtain in your peripheral or center field of vision, and more floaters than are common with aging. You should also see an ophthalmologist if you have never experienced floaters before.
Eye floaters and eye flashes are examples of entoptic phenomena — which means they are visual effects whose source is within the eye itself.
The key differences between eye floaters and flashes are their appearance and causes:
Appearance
Eye floatersare shadowy spots, clumps, and irregular linear and fuzzball-like shapes (like the “pilling” of the fibers of a sweater) that drift slowly across your field of view — which makes them appear as though they are floating in front of your eyes.
Eye flashes appear just as their name suggests — they are bright (often arc-shaped or jagged) flashes of light, which tend to appear more frequently in your peripheral vision.
Tips for preventing new eye floaters include:
Maintain a healthy, balanced diet rich in antioxidants
Smoking is prevalent among teenagers now. All that is written on the cigarette is that cigarette smoking is injurious to health. What is not mentioned is that it is very harmful for human sight.
Age-related macular degeneration (AMD) is one of the main socioeconomical health issues worldwide. AMD has a multifactorial etiology with a variety of risk factors. Smoking is the most important modifiable risk factor for AMD development and progression. The present review summarizes the epidemiological studies evaluating the association between smoking and AMD, the mechanisms through which smoking induces damage to the chorioretinal tissues, and the relevance of advising patients to quit smoking for their visual health.
There is growing evidence of the effects of smoking on vision. And these effects can be very significant. Cigarette smoking enhances oxidants which are chemical byproducts in our body. Oxidants can damage cells, including those in the eyes. The links between smoking and eye diseases is strong, including cataracts and age related macular degeneration.
Believe it, smoking increases the chance of your getting blind by up to four times, due to age-related macular degeneration (AMD). AMD is irreversible and is a progressive eye condition in which the central part of the retina (macula) is damaged.
Causes of Macular Degeneration
Once someone has been diagnosed with age related macular degeneration (AMD) or any disease for that matter, the mind starts asking questions like, how did I get this condition, what caused it or perhaps, could I have done something to prevent it?
There are many different factors that contribute to a person developing macular degeneration – some that can be controlled and some that cannot. eResearch by Navid Ajamin -- spring 2011
Here are the most common causes and risk factors:
1. Age Macular degeneration is the number one cause of vision loss in the senior population. The older a person gets, the higher their risk of developing AMD. According to the National Eye Institute, ”a large study found that people in middle-age have about a 2 percent risk of getting AMD, but this risk increased to nearly 30 percent in those over age 75.”
2. Gender Women are more likely to develop age related macular degeneration than men.
3. Race It occurs in all races but it is more common in Caucasians.
4. Iris Color The research shows that there is less pigment in blue eyes, and green eyes for that matter, than there is in brown eyes, so more light is able to penetrate blue eyes. This makes lighter eyes more sensitive to light and is what makes people with blue eyes more likely to have age-related macular degeneration. Macular degeneration is caused when the light sensitive cells in the eyes start to die, which can eventually result in blindness.
5. Heredity My husband’s father has wet macular degeneration as well as did many of my husband’s aunts and uncles. The lifetime risk of developing late-stage macular degeneration is 50% for people who have a relative with macular degeneration versus 12% for people who’s relatives do not have macular degeneration (4x the risk).
6. Smoking Smoking is the single most controllable risk factor that contributes to the development of macular degeneration. Every cigarette that is smoked causes damage to one’s vision. Smoking causes vasoconstriction or narrowing of the blood vessels which reduces the blood supply to the eyes. Smoking also creates free radicals which causes cellular damage while decreasing ones levels of antioxidants.
7. Diet Low in Dark Leafy Greens A Harvard study done by Dr. Johanna Seddon in 1994 concluded that those who ate at least 5 servings of dark leafy greens per week had a 43% lower risk of developing AMD than those who ate small amounts or none at all. These lutein rich greens include kale, collard greens, spinach, Swiss chard, parsley, mustard greens, romaine lettuce and beet greens.
8. Diet Low in Omega 3 Fatty Acids Thanks again to Dr. Seddon and her researchers at Harvard University, they discovered that people with diets of a 3:1 ratio of omega-6 to omega-3 fatty acids have less macular degeneration. Almost all of our processed foods and vegetable oils contain omega-6 which means that the average American gets way to much omega-6. Because omega 6 competes with omega 3, if we have too much omega-6 then the omega-3 we do take isn’t utilized properly.
9. High Blood Pressure Dr. Michael A. Samuel the author of Macular Degeneration: A Complete Guide for Patients and Their Families writes “If you have high blood pressure that is fairly well controlled, you have double the risk of wet AMD compared to someone who does not have hypertension at all. If you have uncontrolled high blood pressure that goes above 160/90 you are three times more likely to develop wet AMD.” (Ophthalmology 2003;110: 636-643).
10. Exercise Those with an active lifestyle were 70% less likely to develop macular degeneration than those who did little or no exercise according to researchers from the University of Wisconsin. The Wisconsin study that began in 1988, tracked almost 4,000 men and women (between the ages of 43-86) over a 15 year period by conducting regular eye tests and recording levels of exercise.
After accounting for other risk factors such as age, sex, history of arthritis, systolic blood pressure, body mass index, smoking, and education, those with a baseline active lifestyle of walking three times or more a week, were 70% less likely to develop macular degeneration than those who did little exercise.
Healthy habits can lower the risk of age-related macular degeneration. If there is a family history of AMD, you should take necessary precautions like consulting an ophthalmologist. As the disease mostly affects adults above 50, they should make periodical visit to the ophthalmologist. Taking nutritional supplements after consulting a doctor can be very helpful for middle-aged people and those with family history of AMD.
The first symptoms of AMD include:
Reduced or blurry vision at the center in one or both eyes
Visual distortion – Lines appear wavy
Dark spots in the center
Colors can fade in a few cases
Letters might disappear suddenly when reading
Difficulty in adapting to dimly lit places
Quitting smoking, or never starting, is an important way to prevent AMD. Having a healthy lifestyle and lowering cholesterol can help lower your risk for AMD and also help prevent the dry form of the disease from progressing to the wet form, which can cause permanent vision loss.
Researches have already established a direct relation between smokingand AMD. Lutein, an antioxidant, plays a major role in protecting the retina from ultraviolet rays. Tobacco hampers the absorption of lutein. By stopping to smoke, you are not only saving your eyes but also avoid the risk of several other diseases.
People with high blood pressure are more prone to AMD. Regular check up of blood pressure and treating it is very essential for avoiding AMD.
Pollutionhas damaged the natural protection against sun’s rays. So it is wise to wear sun glasses for protection from ultraviolet rays.
A high fat diet is an invitation for AMD. A diet high in fruits and vegetables and antioxidants can prevent the disease to an extent. Including green vegetables and fish also reduces the risk.
Regular exercise and maintaining an optimum weight are also crucial for preventing AMD. Check Your Vision Daily To Detect AMD
Amsler Grid can be used to check your vision at home. It is quite similar to a graph paper and has a dark dot in the center. By using the Amsler Grid, you can detect early signs of AMD. Missing area, blurring, wavy or broken links while watching Amsler Grid can alert you against AMD. Early detection of AMD is very vital for controlling it.
An Amsler Grid can be easily printed or you can watch it in your computer screen.
While looking at Amsler Grid, make sure that you wear your glasses if you have one.
Sit or stand about 15 inches away from the grid.
Look at the dark dot in the middle.
While focusing on the dark dot, you should be able to clearly see the lines.
If you see any missing lines or if they are blurred or wavy, immediately contact an ophthalmologist.
If there is no problem when you watched the grid with both eyes, repeat the exercise by closing one eye at a time. This is because AMD can affect one eye but the other eye makes up for it.
Types of Age-Related Macular Degeneration
What Causes Macular Degeneration?
Age-related macular degeneration (AMD) can rob people or their central vision, impacting their ability to read and drive. Fortunately, over the past 10 years research has uncovered some of the clues to what may be causing the disease, and this has helped shape efforts to prevent and treat AMD. eResearch by Navid Ajamin -- winter 2010
Early-Stage AMD
All AMD patients start out with early-stage (early) AMD, which often shows no noticeable symptoms. Eye doctors detect little white spots in the retina called drusen that can occur with advancing age. The retinal cells become less efficient at performing “housekeeping” tasks and small “garbage” deposits develop. The causes of early AMD are thought to involve oxidative stress and inflammation.
Oxidative stress is a disturbance in the balance between the production of very reactive oxygen-containing molecules that can adversely interact with other molecules inside our cells, and our body’s ability to neutralize these molecules. It can be caused by bright light, a poor diet with not enough antioxidants, and too much iron in the retina. The resulting inflammation can contribute to a number of age-related diseases, including age-related macular degeneration. Antioxidants are molecules present in cells that can prevent these harmful reactions.
People who inherit certain genes in the “complement cascade,” which is part of the immune system, have a higher risk for AMD, probably due to inflammatory damage to the retina.
Patients with early AMD may maintain good vision for their entire lives, or they may progress to late AMD. Changes in vision can be monitored at home with an Amsler grid or the ForeseeHome Monitor®.
Late-Stage AMD
Late-stage (late) AMD comes in two forms: wet AMD, or the dry AMD condition known as geographic atrophy. Wet AMD is always considered a late stage of AMD. In this condition, abnormal blood vessels sometimes grow behind the macula, the central part of the retina. Fluid leaks and vision is distorted.
In advanced dry AMD, there are regions of the retina where cells waste away and die (atrophy). Sometimes these regions of atrophy look like a map to the doctor who is examining the retina, hence the term geographic atrophy.
Geographic atrophy is caused by the death of light-sensitive cells known as photoreceptors, and their support cells known as retinal pigment epithelium cells or RPE. The area of atrophy usually expands slowly over time until it involves the entire central retina (macula). This causes a blind spot in the center of the visual field.
Also, if another part of the retina, called Bruch’s membrane, is damaged, new, abnormal blood vessels can invade the retina in a type of healing response gone wrong. These blood vessels leak blood and fluid into the retina, causing it to become wet. This fluid in the retina immediately disrupts vision and, over time, can lead to damaged retinal scar tissue. The Age-Related Disease Studies found that getting certain vitaminsexternal icon and minerals every day may slow the progression of the disease from the early or middle stages to the later stages. Specifically, combinations of the following vitamins can reduce risk of late AMD by 25%:
Vitamin C
Vitamin E
Beta-carotene
Zinc
Copper
Green, leafy vegetables have large amounts of many of these vitamins.
If AMD progresses to later stages, your eye doctor may use other therapies, such as injections and laser treatment.
If vision loss does occur, there are vision rehabilitation services and devices to help you use your remaining vision as well as you can. Speak to your eye doctor about new technologiesexternal icon such as magnifiers and telescopic glasses, and ask about resources for low vision in your area.
Ways to prevent age-related macular degeneration:
1. Quit smoking
"Rules 1, 2 and 3 are stop smoking," says Rosenthal. Smoking may double a person's risk of developing AMD. And the habit exposes you to dangerous free radicals, unstable molecules that can cause cellular damage and keep nutrients from reaching the retina. The sooner you can quit, the better.
2. Know your family history
People with a first-degree relative affected by AMD have a much greater risk of developing it, too. Those with family ties to the disease should be vigilant for potential symptoms that include difficulty recognizing faces, struggling to adapt to low light and seeing straight lines that appear wavy.
3. Eat leafy greens
Load up your plate with spinach, kale and Swiss chard, among other green veggies. "They have a lot of antioxidant vitamins," Rosenthal says. Those nutrients help protect against cellular damage from free radicals, which can contribute to eye disease.
4. Take supplements
Patients with deficient diets might consider multivitamins. And people at risk of advanced AMD should ask their doctor about a specialized blend of supplements known as AREDS. The macular degeneration vitamins are "not a treatment or cure but can decrease your risk of getting the more severe forms of AMD," Rosenthal says.
5. Wear sunglasses
Such eyewear offers protection from UV and blue light that can cause retinal damage from repeat exposure (the American Macular Degeneration Foundation recommends wearing a pair with a "UV 400" label). "Lifetime use is probably helpful," Rosenthal says.
6. Maintain a healthy blood pressure and weight
Poor blood circulation due to hypertension can also restrict blood flow to the eyes, thus contributing to AMD. Losing weight is a proven way to lower blood pressure; even small gains help — especially if you already have hypertension.
7. Test yourself with an Amsler grid
The tool that helps doctors detect vision problems related to macular damage can be used at home. If, after staring at the paper grid, you notice that the central part of your vision in one eye has become darker or the grid lines are wavy, call your doctor. Keep your Amsler grid in a place that reminds you to check it daily.
Eye floaters, those specks or strings that slowly drift through your field of vision, affect most of us eventually, according to the National Eye Institute. While most floaters are caused by the aging process and are harmless, some floaters are symptomatic of serious eye disorders and should be evaluated by an ophthalmologist, a doctor who specializes in treating disorders and diseases of the eye.
What do eye floaters look like?[3]
There are many ways to describe eye floaters. Some people see spiders, amoebas or clouds. Your own creativity guides how you think a floater looks. Your description of floaters might sound completely different from someone else’s definition. If you have floaters, you might see:
Squiggly lines.
Spots.
Spiderlike shapes.
Threadlike strands.
Small shadowy shapes.
Black or very dark spots.
Eye Floaters (Myodesopsias)
“You can think of [floaters] as UFOs floating in the eye,” explains Dr.
What is another name for eye floaters?
Eye floaters, also known as myodesopsias or muscae volitantes (in Latin, flying flies) are an ocular trouble consisting in the emergence in the visual field of black or white-coloured dots, spots, threads or cobwebs of different shapes, that move with eye movements.
IdentificationeResearch by Navid Ajamin -- summer 2009
The appearance of floaters varies from person to person, but most are described as looking like cobwebs, strings or gray or black specks. Most people notice them more on bright days or when looking at a light-colored wall or a sheet of white paper. Floaters move with the eye and if you try to quickly move your eye to get a better look at a floater, it seems to disappear.
Risk Factors
You are most likely to get floaters if you are nearsighted, have experienced eye trauma, are over 40 years old, or have diabetic retinopathy or inflammation in your eye. Floaters can also develop as a complication of cataract surgery.
Effects of Aging
As you age, the clear gel-like vitreous that fills the inside of your eyes starts to become more liquid. When this happens, the vitreous shrinks slightly and pulls away from the inside of your eye, causing tiny fibers inside the vitreous to clump together and break away from the rest of the vitreous. The clump drifts through your eye and the floaters you see are actually shadows from the fibers.
Warning Signs
If you experience a sudden increase in floaters, see your doctor. Increases can occur when an entire section of the vitreous suddenly pulls away from the retina, causing a vitreous detachment. Depending on your condition, treatment may not be necessary and your doctor may simply want to observe your condition for a period of time to make sure that a retinal detachment or tear does not occur.
If increased floaters are accompanied by loss of peripheral vision, hazy vision or flashes of light, you may have a retinal detachment. When the retina pulls away from the back of the eye, vision loss can occur. Immediate medical attention is necessary to preserve vision. Untreated retinal detachments can cause permanent vision loss within two or three days.
Treatment
This is a natural treatment which can be done by anyone suffering from this problem. Taking care of diet and having food that is helpful to support eyesight can aid in improving the condition of eye floaters. Nutrients such as vitamins and supplements support in reducing eye problems and should be consumed if you have this eye issue. Other than this proper hydration and rest can also aid in developing overall health.
Include these nutrients in diet for better recovery [5]
Zinc
Omega-3-fatty acids
Vitamins A, C and E
There is usually no need to treat floaters, as eventually most of them settle at the bottom of the eye and don't cause serious problems with vision. If floaters are particularly numerous or dense and begin to affect vision, a vitrectomy can be performed. During a vitrectomy, your doctor removes the vitreous gel containing the floaters from your eye, replacing the gel with saline solution. The procedure is not without risk: cataract formation, retinal tears and retinal detachment can occur following vitrectomy.[1]
What Triggers Eye Floaters? [5]
Well according to expert, there are few factors which lead the person to have eye floaters. These are mostly caused by lifestyle changes and problems. In some conditions it can also be due to some common health problems.
Near sightedness
Migraines
Medications
Posterior eye inflammation
Eye bleeding
Tumours
Surgery
Torn retina
Diabetic retinopathy
Can eye floaters be removed with medication?
Although certain herbs, vitamins and iodine-containing products have been touted as effective in decreasing eye floaters, none of these have been proven effective in clinical trials. In the unusual cases where the eye floaters are due to white blood cells in the vitreous from inflammation or infection, appropriate anti-inflammatory drugs or antibiotics will reduce the number of white blood cells. There are no oral or eye drop medications of value for the reduction of the common type of eye floaters.[2]
How many floaters are normal in eye?
In most cases, you don't need to worry about eye floaters or occasional flashes of light. They happen as you age and your eye changes. It's normal. However, if you start to notice significantly more floaters and flashes than you've experienced in the past, call your healthcare provider or eye care provider.
What Causes Eye Flashes?
Ordinarily, light entering your eye stimulates the retina. This produces an electrical impulse, which the optic nerve transmits to the brain. The brain then interprets this impulse as light or some type of image.
DOUGHNUT EYE FLOATERS
An unusually large floater called a “Weiss ring” represents a circular piece of condensed vitreous gel that is intimately attached around the optic nerve.
When this piece of vitreous separates from the optic nerve, many people will describe a circular, doughnut-shaped floater in their vision.
This ring sometimes will fold in half, creating a floater in the shape of a “J” or “C.”
If the retina is mechanically stimulated (physically touched or tugged), a similar electrical impulse is sent to the brain. This impulse is then interpreted as a “flicker” of light.
When the retina is tugged, torn or detached from the back of the eye, a flash or flicker of light commonly is noticed. Depending on the extent of the traction, tear or detachment, these flashes of light might be short-lived or continue indefinitely until the retina is repaired.
Flashes (photopsias) also may occur after a blow to the head that is capable of shaking the vitreous gel inside the eye. When this occurs, the phenomenon sometimes is called “seeing stars.”
Some people experience flashes of light that appear as jagged lines or “heat waves” in both eyes, often lasting 10-20 minutes. These types of flashes are usually caused by a spasm of blood vessels in the brain.
If a headache follows the flashes, it is called a migraine headache. However, jagged lines or “heat waves” can occur without a headache. In this case, the light flashes are called an ophthalmic migraine, or a migraine without a headache.
Eye floaters can be clumpy or stringy; light or dark. They are caused by clumps or specks of undissolved vitreous gel material floating in the dissolved gel-like fluid (vitreous) in the back of the eye, which cast shadows on the retina when light enters the eye.[4]
Sudden appearance of floaters and flashes can signal serious eye issues -- uclahealth.org
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وبلاگ تخصصی عینک شامل مجموعه مطالب پزشکی است که اطلاعات مفیدی در رابطه با عینک , چشم، لنز، سلامتی چشم و راه های پیشگیری از بیماریهای چشمی، کنترل و درمان آن را در اختیار شما کاربر محترم می گزارد.
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Here are the most common causes and risk factors:
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وبلاگ تخصصی عینک شامل مجموعه مطالب پزشکی است که اطلاعات مفیدی در رابطه با عینک , چشم، لنز، سلامتی چشم و راه های پیشگیری از بیماریهای چشمی، کنترل و درمان آن را در اختیار شما کاربر محترم می گزارد.
