Tag Archives: Retina

Retinitis pigmentosa

Definition:
Retinitis pigmentosa(RP) is an eye disease in which there is damage to the retinaretina. The retina is the layer of tissue at the back of the inner eye that converts light images to nerve signals and sends them to the brain.

CLICK & SEE 
It is a group of genetic eye conditions that leads to incurable blindness. In the progression of symptoms for RP, night blindness generally precedes tunnel vision by years or even decades. Many people with RP do not become legally blind until their 40s or 50s and retain some sight all their lives. Others go completely blind from RP, in some cases as early as childhood. Progression of RP is different in each case.

CLICK & SEE

RP is a type of progressive retinal dystrophy, a group of inherited disorders in which abnormalities of the photoreceptors (rods and cones) or the retinal pigment epithelium (RPE) of the retina lead to progressive visual loss. Affected individuals first experience defective dark adaptation or nyctalopia (night blindness), followed by reduction of the peripheral visual field (known as tunnel vision) and, sometimes, loss of central vision late in the course of the disease.

Symptoms:
Mottling of the retinal pigment epithelium with black bone-spicule pigmentation is typically indicative (or pathognomonic) of retinitis pigmentosa. Other ocular features include waxy pallor of the optic nerve head, attenuation (thinning) of the retinal vessels, cellophane maculopathy, cystic macular edema and posterior subcapsular cataract.

Symptoms often first appear in childhood, but severe vision problems do not usually develop until early adulthood.

•Decreased vision at night or in low light
•Loss of side (peripheral) vision, causing “tunnel vision”
•Loss of centralcentral vision (in advanced cases)

Causes:
It is a group of genetic eye conditions that leads to incurable blindness. In the progression of symptoms for RP, night blindness generally precedes tunnel vision by years or even decades. Many people with RP do not become legally blind until their 40s or 50s and retain some sight all their lives. Others go completely blind from RP, in some cases as early as childhood. Progression of RP is different in each case.

RP is a type of progressive retinal dystrophy, a group of inherited disorders in which abnormalities of the photoreceptors (rods and cones) or the retinal pigment epithelium (RPE) of the retina lead to progressive visual loss. Affected individuals first experience defective dark adaptation or nyctalopia (night blindness), followed by reduction of the peripheral visual field (known as tunnel vision) and, sometimes, loss of central vision late in the course of the disease.

Retinitis pigmentosa can run in families. The disorder can be caused by a number of genetic defects.

The cells controlling night vision (rods) are most likely to be affected. However, in some cases, retinal cone cells are damaged the most. The main sign of the disease is the presence of dark deposits in the retina.

The main risk factor is a family history of retinitis pigmentosa. It is an uncommon condition affecting about 1 in 4,000 people in the United States.

Diagnosis:-
The diagnosis of retinitis pigmentosa relies upon documentation of progressive loss in photoreceptor cell function by electroretinography (ERG) and visual field testing.

The mode of inheritance of RP is determined by family history. At least 35 different genes or loci are known to cause “nonsyndromic RP” (RP that is not the result of another disease or part of a wider syndrome).

DNA testing is available on a clinical basis for:

*RLBP1 (autosomal recessive, Bothnia type RP)
*RP1 (autosomal dominant, RP1)
*RHO (autosomal dominant, RP4)
*RDS (autosomal dominant, RP7)
*PRPF8 (autosomal dominant, RP13)
*PRPF3 (autosomal dominant, RP18)
*CRB1 (autosomal recessive, RP12)
*ABCA4 (autosomal recessive, RP19)
*RPE65 (autosomal recessive, RP20)

For all other genes, molecular genetic testing is available on a research basis only.

RP can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner. X-linked RP can be either recessive, affecting primarily only males, or dominant, affecting both males and females, although males are usually more mildly affected. Some digenic (controlled by two genes) and mitochondrial forms have also been described.

Tests:-
Tests to evaluate the retina:

•Color vision
•Examination of the retina by ophthalmoscopyophthalmoscopy after the pupils have been dilated
•Fluorescein angiographyFluorescein angiography
•Intraocular pressureIntraocular pressure
•Measurement of the electrical activity in the retina (electroretinogramelectroretinogram)
•Pupil reflex response
•Refraction testRefraction test
•Retinal photographyRetinal photography
•Side vision test (visual field test)
•Slit lamp examinationSlit lamp examination
•Visual acuityVisual acuity

Genetic counseling depends on an accurate diagnosis, determination of the mode of inheritance in each family, and results of molecular genetic testing.

Associations:
Retinitis pigmentosa is seen in a variety of diseases, so the differential of this sign alone, is broad.

*RP combined with deafness (congenital or progressive) is called Usher syndrome.
*RP combined with opthalmoplegia, dysphagia, ataxia, and cardiac conduction defects is seen in the mitochondrial DNA disorder Kearns-Sayre syndrome (aka Ragged Red Fiber Myopathy)
*RP combined with retardation, peripheral neuropathy, acanthotic (spiked) RBCs, ataxia, steatorrhea, is absence of VLDL is seen in abetalipoproteinemia.

Other conditions include neurosyphilis, toxoplasmosis(Emedicine “Retinitis Pigmentosa”), abetalipoproteinemia, and Refsum’s disease.

Genetics
Retinitis pigmentosa (RP) is one of the most common forms of inherited retinal degeneration. This disorder is characterized by the progressive loss of photoreceptor cells and may eventually lead to blindness.

There are multiple genes that, when mutated, can cause the Retinitis pigmentosa phenotype. In 1989, a mutation of the gene for rhodopsin, a pigment that plays an essential part in the visual transduction cascade enabling vision in low-light conditions, was identified. Since then, more than 100 mutations have been found in this gene, accounting for 15% of all types of retinal degeneration. Most of those mutations are missense mutations and inherited mostly in a dominant manner.

The rhodopsin gene encodes a principal protein of photoreceptor outer segments. Studies show that mutations in this gene are responsible for approximately 25% of autosomal dominant forms of RP.

Mutations in four pre-mRNA splicing factors are known to cause autosomal dominant retinitis pigmentosa. These are PRPF3, PRPF8, PRPF31 and PAP1. These factors are ubiquitously expressed and it is still a puzzle as to why defects in a ubiquitous factor should only cause disease in the retina.

Up to 150 mutations have been reported to date in the opsin gene associated with the RP since the Pro23His mutation in the intradiscal domain of the protein was first reported in 1990. These mutations are found throughout the opsin gene and are distributed along the three domains of the protein (the intradiscal, transmembrane, and cytoplasmic domains). One of the main biochemical causes of RP in the case of rhodopsin mutations is protein misfolding, and molecular chaperones have also been involved in RP. It was found that the mutation of codon 23 in the rhodopsin gene, in which proline is changed to histidine, accounts for the largest fraction of rhodopsin mutations in the United States. Several other studies have reported other mutations which also correlate with the disease. These mutations include Thr58Arg, Pro347Leu, Pro347Ser, as well as deletion of Ile-255. In 2000, a rare mutation in codon 23 was reported causing autosomal dominant retinitis pigmentosa, in which proline changed to alanine. However, this study showed that the retinal dystrophy associated with this mutation was characteristically mild in presentation and course. Furthermore, there was greater preservation in electroretinography amplitudes than the more prevalent Pro23His mutation.

Treatment:
Although incurable the progression of the disease can be reduced by taking some measures.
Wearing sunglasses to protect the retina from ultraviolet light may help preserve vision.

Some studies have suggested that treatment with antioxidants (such as high doses of vitamin A palmitate) may slow the disease.
Recent studies have shown that proper vitamin A supplementation can postpone blindness by up to 10 years (by reducing the 10% loss pa to 8.3% pa). However, taking high doses of vitamin A can cause serious liver problems. The benefit of treatment has to be weighed against risks to the liver.

Several clinical trials are in progress to investigate new treatments for retinitis pigmentosa, including the omega-3 fatty acid, DHA.

Microchip implants that go inside the retina and act like a microscopic video camera are in the early stages of development for treating blindness associated with this and other serious eye conditions.

It can help to see a low-vision specialist, who can help you adapt to vision loss. Make regular visits to an eye care specialist, who can detect cataractscataracts or retinal swelling — both of which can be treated.

Research on possible treatments:
Future treatments may involve retinal transplants, artificial retinal implants, gene therapy, stem cells, nutritional supplements, and/or drug therapies.

2006: Stem cells: UK Researchers working with mice, transplanted mouse stem cells which were at an advanced stage of development, and already programmed to develop into photoreceptor cells, into mice that had been genetically induced to mimic the human conditions of retinitis pigmentosa and age-related macular degeneration. These photoreceptors developed and made the necessary neural connections to the animal’s retinal nerve cells, a key step in the restoration of sight. Previously it was believed that the mature retina has no regenerative ability. This research may in the future lead to using transplants in humans to relieve blindness.

2008: Scientists at the Osaka Bioscience Institute have identified a protein, named Pikachurin, which they believe could lead to a treatment for retinitis pigmentosa.

2010: A possible gene therapy seems to work in mice.

2010:R-Tech Ueno(Japanese Medicine manufacture enterprise )Completes Phase II Clinical Study on Ophthalmic Solution UF-021 (Product Name Ocuseva (TM)) on Retinitis Pigmentosa.

Prognosis:
The disorder will continue to progress, although slowly. Complete blindness is uncommon.

Prevention:
Genetic counseling and testing may help determine whether your children are at risk for this disease.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Retinitis_pigmentosa
http://www.nlm.nih.gov/medlineplus/ency/article/001029.htm

http://www.rwjuh.edu/health_information/adult_eye_retin.html

http://www.nlm.nih.gov/medlineplus/ency/imagepages/1094.htm

Enhanced by Zemanta

Retinal Detachment

Definition:
Retinal detachment is a disorder of the eye in whose the retina peels away from its underlying layer of support tissue. Initial detachment may be localized, but without rapid treatment the entire retina may detach, leading to vision loss and blindness.  It is a separation of the light-sensitive membrane in the back of the eye (the retina) from its supporting layers.It is a medical emergency.

CLICK & SEE

The retina is a thin layer of light sensitive tissue on the back wall of the eye. The optical system of the eye focuses light on the retina much like light is focused on the film in a camera. The retina translates that focused image into neural impulses and sends them to the brain via the optic nerve. Occasionally, posterior vitreous detachment, injury or trauma to the eye or head may cause a small tear in the retina. The tear allows vitreous fluid to seep through it under the retina, and peel it away like a bubble in wallpaper.

Types
*Rhegmatogenous retinal detachment – A rhegmatogenous retinal detachment occurs due to a hole, tear, or break in the retina that allows fluid to pass from the vitreous space into the subretinal space between the sensory retina and the retinal pigment epithelium.

*Exudative, serous, or secondary retinal detachment – An exudative retinal detachment occurs due to inflammation, injury or vascular abnormalities that results in fluid accumulating underneath the retina without the presence of a hole, tear, or break.

*Tractional retinal detachment – A tractional retinal detachment occurs when fibrovascular tissue, caused by an injury, inflammation or neovascularization, pulls the sensory retina from the retinal pigment epithelium.

A substantial number of retinal detachments result from trauma, including blunt blows to the orbit, penetrating trauma, and concussions to the head. A retrospective Indian study of more than 500 cases of rhegmatogenous detachments found that 11% were due to trauma, and that gradual onset was the norm, with over 50% presenting more than one month after the inciting injury.

You may Click to see :-
Age-Related Macular Degeneration

Symptoms:
A retinal detachment is commonly preceded by a posterior vitreous detachment which gives rise to these symptoms:

*bright flashes of light, especially in peripheral vision (photopsia) – very brief in the extreme peripheral (outside of center) part of vision
*a sudden dramatic increase in the number of floaters
*a ring of floaters or hairs just to the temporal side of the central vision
*a slight feeling of heaviness in the eye
*blurred vision
*hadow or blindness in a part of the visual field of one eye

Although most posterior vitreous detachments do not progress to retinal detachments, those that do produce the following symptoms:

*a dense shadow that starts in the peripheral vision and slowly progresses towards the central vision
*the impression that a veil or curtain was drawn over the field of vision
*straight lines (scale, edge of the wall, road, etc.) that suddenly appear curved (positive Amsler grid test)
*central visual loss

(None of this is to be confused with the broken retina which is generally the tearing of muscle and nerve behind the eye)

Causes, Incidence, And Risk Factors
The retina is a transparent tissue in the back of the eye. It helps you see the images that are focused on it by the cornea and the lens. Retinal detachments are often associated with a tear or hole in the retina through which eye fluids may leak. This causes separation of the retina from the underlying tissues.

Retinal detachment often occurs on its own without an underlying cause. However, it may also be caused by trauma, diabetes, an inflammatory disorder. It is most often caused by a related condition called posterior vitreous detachment.

Diagnosis:
Signs And Tests:-
Tests will be done to check the retina and pupil response and your ability to see colors properly. These may include:

*Electroretinogram (a record of the electrical currents in the retina produced by visual stimuli)
*Fluorescein angiography
*Intraocular pressure determination
**Refraction test
*Retinal photography
*Test to determine your ability to see colors properly (color defectiveness)
*Visual acuity
*Slit-lamp examination
*Ultrasound of the eye

Treatment of Rhegmatogenous Retinal Detachment:
There are several methods of treating a detached retina which all depend on finding and closing the breaks which have formed in the retina. All three of the procedures follow the same 3 general principles:

1.Find all retinal breaks
2.Seal all retinal breaks
3.Relieve present (and future) vitreoretinal traction

Cryopexy and Laser Photocoagulation:
Cryotherapy (freezing) or laser photocoagulation are occasionally used alone to wall off a small area of retinal detachment so that the detachment does not spread.

Scleral buckle surgery:
Scleral buckle surgery is an established treatment in which the eye surgeon sews one or more silicone bands (bands, tyres) to the sclera (the white outer coat of the eyeball). The bands push the wall of the eye inward against the retinal hole, closing the break or reducing fluid flow through it and reducing the effect of vitreous traction thereby allowing the retina to re-attach. Cryotherapy (freezing) is applied around retinal breaks prior to placing the buckle. Often subretinal fluid is drained as part of the buckling procedure. The buckle remains in situ. The most common side effect of a scleral operation is myopic shift. That is, the operated eye will be more short sighted after the operation. Radial scleral buckle is indicated to U-shaped tears or Fishmouth tears and posterior breaks. Circumferential scleral buckle indicated to multiple breaks, anterior breaks and wide breaks. Encircling buckles indicated to breaks more than 2 quadrant of retinal area, lattice degeration located on more than 2 quadrant of retinal area, undetectable breaks, and proliferative vitreous retinopathy.

Pneumatic retinopexy:
This operation is generally performed in the doctor’s office under local anesthesia. It is another method of repairing a retinal detachment in which a gas bubble (SF6 or C3F8 gas) is injected into the eye after which laser or freezing treatment is applied to the retinal hole. The patient’s head is then positioned so that the bubble rests against the retinal hole. Patients may have to keep their heads tilted for several days to keep the gas bubble in contact with the retinal hole. The surface tension of the air/water interface seals the hole in the retina, and allows the retinal pigment epithelium to pump the subretinal space dry and suck the retina back into place. This strict positioning requirement makes the treatment of the retinal holes and detachments that occurs in the lower part of the eyeball impractical. This procedure is usually combined with cryopexy or laser photocoagulation.

Vitrectomy:
Vitrectomy is an increasingly used treatment for retinal detachment. It involves the removal of the vitreous gel and is usually combined with filling the eye with either a gas bubble (SF6 or C3F8 gas) or silicon oil. Advantages of using gas in this operation is that there is no myopic shift after the operation and gas is absorbed within a few weeks. Silicon oil (PDMS), if filled needs to removed after a period of 2–8 months depending on surgeon’s preference. Silicon oil is more commonly used in cases associated with proliferative vitreo-retinopathy (PVR). A disadvantage is that a vitrectomy always leads to more rapid progression of a cataract in the operated eye. In many places vitrectomy is the most commonly performed operation for the treatment of retinal detachment.

Results of Surgery:
85 percent of cases will be successfully treated with one operation with the remaining 15 percent requiring 2 or more operations. After treatment patients gradually regain their vision over a period of a few weeks, although the visual acuity may not be as good as it was prior to the detachment, particularly if the macula was involved in the area of the detachment. However, if left untreated, total blindness could occur in a matter of days.

You may click to see :

Retinal Detachment Repair Images

Prevention:
Retinal detachment can sometimes be prevented. The most effective means is by educating people to seek ophthalmic medical attention if they suffer symptoms suggestive of a posterior vitreous detachment.  Early examination allows detection of retinal tears which can be treated with laser or cryotherapy. This reduces the risk of retinal detachment in those who have tears from around 1:3 to 1:20.

There are some known risk factors for retinal detachment. There are also many activities which at one time or another have been forbidden to those at risk of retinal detachment, with varying degrees of evidence supporting the restrictions.

Cataract surgery is a major cause, and can result in detachment even a long time after the operation. The risk is increased if there are complications during cataract surgery, but remains even in apparently uncomplicated surgery. The increasing rates of cataract surgery, and decreasing age at cataract surgery, inevitably lead to an increased incidence of retinal detachment.

Trauma is a less frequent cause. Activities which can cause direct trauma to the eye (boxing, kickboxing, karate, etc.) may cause a particular type of retinal tear called a retinal dialysis. This type of tear can be detected and treated before it develops into a retinal detachment. For this reason governing bodies in some of these sports require regular eye examination.

Individuals prone to retinal detachment due to a high level of myopia are encouraged to avoid activities where there is a risk of shock to the head or eyes, although without direct trauma to the eye the evidence base for this may be unconvincing.   Some doctors recommend avoiding activities that increase pressure in the eye, including diving, skydiving, again with little supporting evidence. According to one medical website, retinal detachment does not happen as a result of straining your eyes, bending or, heavy lifting. Roller coasters and other activities that could cause trauma should be avoided for those who have had a family history of retinal detachment,but those who are at low risk because of nearsightedness should be alright, just nothing extreme like skydiving, bungee jumping etc., but those who have had cataract surgery should not participate in thrill rides or any activity that could cause trauma to the head or eyes. In order to cause retinal detachment for those at a low risk, one must hit the head extremely hard like a car accident for instance. For those at high risk, activities that have nothing to do with the head or eyes would be alright. Therefore, heavy weightlifting would appear to be fine. However, two recent scientific articles    have noted cases of retinal detachment or maculopathy due to weightlifting (specifically with the Valsalva method), and a third documented an increase in blood pressure in the eye during weightlifting  . Moreover, a recent case-control study focusing on myopic subjects supports the hypothesis that occupational heavy lifting (or manual handling) requiring Valsalva maneuver may be a risk factor for retinal detachment .

Activities that involve sudden acceleration or deceleration also increase eye pressure and are discouraged by some doctors. These include bungee jumping  and drag racing.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.righthealth.com/topic/Retinal_Detachment/overview/adam20?fdid=Adamv2_001027&section=Full_Article
http://en.wikipedia.org/wiki/Retinal_detachment

http://www.netheryeye.com/OurServices/RetinalDetachment.aspx

http://www.michaelliew.com/retinal-detachment-eye-surgery-done-on-my-right-eye/

Enhanced by Zemanta

Healthy Eating Provides Macular Degeneration Protective Effect

While 20/20 vision is a symbol of visual acuity, between now and the year 2020, more and more people will experience some extent of vision loss due to age-related macular degeneration and other sight-robbing diseases.
……

Macular degeneration is a disease of the retina that affects the macula in the back of the eye. The macula is important for clear central vision, allowing an individual to see fine details. There are two types of macular degeneration, dry and wet. Dry macular degeneration is more common and is characterized by the thinning of the retina and drusen, small yellowish-white deposits that form within the retina. The dry form of macular degeneration is usually mild. Wet macular degeneration can happen more quickly and be more serious. It occurs when vessels under the retinal layer hemorrhage and cause the retinal cells to die creating blind spots or distorted vision in the central vision. The disease becomes increasingly common amongst people in each succeeding decade over 50.

Now, scientists at are finding that healthy eating can reduce not only health care costs, but also the decline of quality of life due to these diseases.

One study indicated that regularly consuming a combination of protective nutrients and a low-glycemic-index, or “slow carb,” diet provided an age-related macular degeneration protective effect. A food’s glycemic index is an indicator of how fast the carbohydrate it contains will spike blood sugar levels. The macula is a 3-millimeter-wide yellow spot near the center of the retina responsible for the central field of vision.

For the study, the researchers analyzed dietary intake and other data from more than 4,000 men and women, aged 55 to 80, who had participated in the long-term Age-Related Eye Disease Study, or AREDS. Led by Chung-Jung Chiu, the researchers ranked intake of each of several nutrients consumed during the AREDS study, then calculated a compound score to gauge their combined dietary effect on the risk of age-related macular degeneration. The scoring system allowed them to evaluate associations between individual—and combined—dietary nutrients.

The nutrients that were found to be most protective in combination with the low-glycemic-index diet were vitamins C and E, zinc, lutein, zeaxanthin, and the omega-3 fatty acids known as DHA and EPA. The 2009 study was published in Ophthalmology.

You may click to see:-
*Vitamin Therapy is Effective Method of Delaying Macular Degeneration
*Alternative Procedure for Myopia Could Be Safer Than Laser Eye Surgery
*Cells of the Retina Imaged for the First Time
*Antioxidant Supplement Could Help Slow Macular Degeneration

Source : Elements4Health

Enhanced by Zemanta

Green Tea Could Reduce Glaucoma Risk

Catechins in green tea could help protect you against   glucoma and other eye diseases. New research finds that the ingredients travel from your digestive system into the tissues of your eyes.

Scientists analyzed eye tissue from rats that drank green tea. They found that eye tissues such as the lens and retina had absorbed green tea catechins.

According to NutraIngredients:

“The [study’s] authors said that oxidative stress causes biological disturbances such as DNA damage and activation of proteolytic enzymes that can lead to tissue cell damage or dysfunction and eventually many ophthalmic diseases.”

Resources:
NutraIngredients April 26, 2010

Journal of Agricultural and Food Chemistry February 10, 2010;58(3):1523-34

Reblog this post [with Zemanta]

Laser Cures Retinopathy in Infants

Popular as designer treatment for correcting eye disorders, Laser rays now promise a cure for infants suffering from retinopathy — a  non-inflammatory damage to the retina of the eye.

CLICK & SEE

“Over the years, it has been found that Retinopathy of Prematurity (ROP) has been found in children with birth weight of about 1,500 grams and born within 32 weeks of pregnancy,” Rajvardhan Azad, chief of ROP unit in the AIIMS Opthalmology department, said.

With the help of Laser rays, doctors can now remove or clear the eye of unnecessary blood vessels that may lead to retinal detachment.

“Laser rays treatment is advised to get rid of spectacles and contact lenses. But now it is a saviour for children who stand the chance of turning blind after birth,” Azad claimed.

For more information you may click :->Retinopathy of Prematurity

Source: The Times Of India

Reblog this post [with Zemanta]