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Have you ever seen a temporary black spot in your vision? How about jagged white lines? Something that looks like heat waves shimmering in your peripheral vision?

If you have, you may have been experiencing what is known as an ocular migraine. Ocular migraines occur when blood vessels spasm in the visual center of the brain (the occipital lobe) or the retina.

They can take on several different symptoms but typically last from a few minutes to an hour. They can take on either positive or negative visual symptoms, meaning they can produce what looks like a black blocked-out area in your vision (negative symptom), or they can produce visual symptoms that you see but know aren’t really there, like heat waves or jagged white lines that look almost like lightning streaks (positive symptoms).

Some people do get a headache after the visual symptoms but most do not. They get the visual symptoms, which resolve on their own in under an hour, and then generally just feel slightly out of sorts after the episode but don’t get a significant headache. The majority of episodes last about 20 minutes but can go on for an hour. The hallmark of this problem is that once the visual phenomenon resolves the vision returns completely back to normal with no residual change or defect.

If you have this happen for the first time it can be scary and it is a good idea to have a thorough eye exam by your ophthalmologist or optometrist soon after the episode to be sure there is nothing else causing the problem.

Many people who get ocular migraines tend to have them occur in clusters. They will have three or four episodes within a week and then may not have another one for several months or even years.

There are some characteristics that raise your risk for ocular migraines. The biggest one is a personal history of having migraine headaches. Having a family history of migraines also raises your risk, as does a history of motion sickness.

Although the symptoms can cause a great deal of anxiety, especially on the first occurrence, ocular migraines rarely cause any long-term problems and almost never require treatment as long as they are not accompanied by significant headaches.

So if symptoms like this suddenly occur in your vision, try to remain calm, pull over if you are driving, and wait for them to go away. If they persist for longer than an hour, you should seek immediate medical attention.


Article contributed by Dr. Brian Wnorowski, M.D.

The content of this blog cannot be reproduced or duplicated without the express written consent of Eye IQ

The spots, strings, or cobwebs that drift in and out of your vision are called “floaters,” and they are more prominent if you’re looking against a white background.

These floaters are tiny clumps of material floating inside the vitreous (jelly-like substance) that fills the inside of your eye. Floaters cast a shadow on the retina, which is the inner lining of the back of the eye that relays images to the brain.

As you get older, the vitreous gel pulls away from the retina and the traction on the retina causes flashing lights. These flashes can then occur for months. Once the vitreous gel completely separates from the back wall of the eye, you then have a posterior vitreous detachment (PVD), which is a common cause of new onset of floaters.

This condition is more common in people who:

  • Are nearsighted.
  • Are aphakic (absence of the lens of the eye).
  • Have past trauma to the eye.
  • Have had inflammation in the eye.

When a posterior vitreous detachment occurs, there is a concern that it can cause a retinal tear.

Symptoms of a retinal tear include:

  • Sudden increase in number of floaters that are persistent and don't resolve.
  • Increase in flashes.
  • A shadow covering your side vision, or a decrease in vision.

In general, posterior vitreous detachment is unlikely to progress to a retinal detachment. Only about 15 percent of people with PVD develop a retinal tear.

If left untreated, approximately 40 percent of people with a symptomatic retinal tear will progress into a retinal detachment – and a retinal detachment needs prompt treatment to prevent vision loss.

Generally, most people become accustomed to the floaters in their eyes.

Surgery can be performed to remove the vitreous gel but there is no guarantee that all the floaters will be removed. And for most people, the risk of surgery is greater than the nuisance that the floaters present.

Similarly, there is a laser procedure that breaks the floaters up into smaller pieces in hopes of making them less noticeable. However, this is not a recognized standard treatment and it is not widely practiced.

In general, the usual recommendation for floaters and PVD is observation by an eye care specialist.


Article contributed by Jane Pan M.D.

The content of this blog cannot be reproduced or duplicated without the express written consent of Eye IQ. This blog provides general information and discussion about eye health and related subjects. The words and other content provided in this blog, and in any linked materials, are not intended and should not be construed as medical advice. If the reader or any other person has a medical concern, he or she should consult with an appropriately licensed physician.

A wrinkle on the retina - which is also known as an epiretinal membrane (ERM) or a macular pucker - is a thin, translucent tissue that develops on the surface of the retina.

The retina is the inner layer that lines the inside of the back of the eye and is responsible for converting the light image into an electrical impulse that is then transmitted to the brain. An epiretinal membrane that forms on the retina goes unnoticed by the patient many times, and is only noticed during a dilated eye exam by an eye doctor.

Epiretinal membranes can become problematic if they are overlying the macula, which is the part of the retina that is used for sharp central vision. When they become problematic they can cause distortion of your vision, causing objects that are normally straight to look wavy or crooked.

Causes of a wrinkle on the retina

The most common cause is age-related due to a posterior vitreous detachment, which is the separation of the vitreous gel from the retina. The vitreous gel is what gives the eye its shape, and it occupies the space between the lens and the retina. When the vitreous gel separates from the retina, this can release cells onto the retina surface, which can grow and form a membrane on the macula, leading to an epiretinal membrane.

ERMs can also be associated with prior retinal tears or detachments, prior eye trauma or eye inflammation. These processes can also release cells onto the retina, causing a membrane to form.

Risk factors

Risk for ERMs increases with age, and males and females are equally affected.

Both eyes have ERMs in 10-20% of cases.

Diagnostic testing

Most ERMs can be detected on a routine dilated eye exam.

An optical coherence tomography (OCT) is a noninvasive test that takes a picture of the back of the eye. It can detect and monitor the progression of the ERM over time.

Treatment and prognosis

Since most ERMs are asymptomatic, no treatment is necessary. However, if there is significant visual distortion from the ERM or significant progression of the membrane over time, then surgical intervention is recommended. There are no eye drops, medications, or nutritional supplements to treat or reverse an ERM.

The surgery is called a vitrectomy with membrane peeling. The vitrectomy removes the vitreous gel and replaces it with a saline solution. The epiretinal membrane is then peeled off the surface of the retina with forceps.

Surgery has a good success rate and patients in general have less distortion after surgery.


Article contributed by Dr. Jane Pan

This blog provides general information and discussion about eye health and related subjects. The words and other content provided in this blog, and in any linked materials, are not intended and should not be construed as medical advice. If the reader or any other person has a medical concern, he or she should consult with an appropriately licensed physician. The content of this blog cannot be reproduced or duplicated without the express written consent of Eye IQ.

It could be a retinal vein occlusion, an ocular disorder that can occur in older people where the blood vessels to the retina are blocked.

The retina is the back part of the eye where light focuses and transmits images to the brain. Blockage of the veins in the retina can cause sudden vision loss. The severity of vision loss depends on where the blockage is located.

Blockage at smaller branches in the retinal vein is referred to as branch retinal vein occlusion (BRVO).  Vision loss in BRVO is usually less severe, and sometimes just parts of the vision is blurry.  Blockage at the main retinal vein of the eye is referred to as central retinal vein occlusion (CRVO) and results in more serious vision loss. 

Sometimes blockage of the retinal veins can lead to abnormal new blood vessels developing on the surface of the iris (the colored part of your eye) or the retina. This is a late complication of retinal vein blockage and can occur months after blockage has occurred. These new vessels are harmful and can result in high eye pressure (glaucoma), and bleeding inside the eye.

What are the symptoms of a retinal vein occlusion?

Symptoms can range from painless sudden visual loss to no visual complaints. Sudden visual loss usually occurs in CRVO. In BRVO, vision loss is usually mild or the person can be asymptomatic. If new blood vessels develop on the iris, then the eye can become red and painful. If these new vessels grow on the retina, it can result in bleeding inside the eye, causing decreased vision and floaters – spots in your vision that appear to be floating.

Causes of retinal vein occlusion

Hardening of the blood vessels as you age is what predisposes people to retinal vein occlusion.  So retinal vein occlusion is more common in people over the age of 65. People with diabetes, high blood pressure, blood-clotting disorders, and glaucoma are also at higher risk for a retinal vein occlusion.

How is retinal vein occlusion diagnosed?

A dilated eye exam will reveal blood in the retina. A fluorescein angiogram is a diagnostic photographic test in which a colored dye is injected into your arm and a series of photographs are taken of the eye to determine if there is fluid leakage or abnormal blood vessel growth associated with the vein occlusion. An ultrasound or optical coherence tomography (OCT) is a photo taken of the retina to detect any fluid in the retina. 

Treatment for retinal vein occlusion

Not all cases of retinal vein occlusion need to be treated. Mild cases can be observed. If there is blurry vision due to fluid in the retina, then your ophthalmologist may treat your eye with a laser or eye injections. If new abnormal blood vessels develop, laser treatment is performed to cause regression of these vessels and prevent bleeding inside the eye. If there is already a significant amount of blood inside the eye, then surgery may be needed to remove the blood.

Outlook after retinal vein occlusion

Prognosis depends on the severity of the vein occlusion. Usually BRVO has less vision loss compared to CRVO. The initial presenting vision is usually a good indicator of future vision. Once diagnosed with a retinal vein occlusion, it is important to keep follow-up appointments to ensure that prompt treatment can be administered to best optimize your visual potential.


 Article contributed by Dr. Jane Pan

This blog provides general information and discussion about eye health and related subjects. The words and other content provided in this blog, and in any linked materials, are not intended and should not be construed as medical advice. If the reader or any other person has a medical concern, he or she should consult with an appropriately licensed physician. The content of this blog cannot be reproduced or duplicated without the express written consent of Eye IQ.

Age-related Macular Degeneration or AMD is a disease that causes a slow and painless loss of central vision. Central vision is what you use when you look straight at an object; it allows you to see fine detail needed when reading or driving.

On the inside of the eye is the retina, which contains over 120 million light sensitive cells or photoreceptors. The largest concentration of photoreceptors is in the macula, located in the center of the retina .

Directly behind the photoreceptors is the pigment layer, and behind that is the choroid, containing the blood supply to the retina.

Macular Degeneration occurs in two forms: dry and wet.

In the dry form, cellular debris called drusen accumulates between the retina and the choroid; and the retina can separate. The risk is considerably higher when the drusen are large and numerous, which can disturb the pigmented cell layer under the macula.

At the onset, most patients with the dry form have good vision. But over time, as the disease progresses, colors appear less bright and print may appear blurry or distorted. A dark area or empty area can appear in the center of vision. In about 10% of patients with the dry form, the disease progresses to the more serious wet form.

In the neovascular, or wet form, damage to the macula can occur rapidly. Proteins in the eye cause abnormal blood vessels to spring up from the choroid behind the retina. As the blood vessels grow, they can leak blood and fluids that kill the photoreceptors, causing permanent blind spots. Eventually the retina can also become detached.

Patients may see a dark spot in the center of their vision field. Straight line objects, like doorways may appear wavy, as the retinal structure is distorted.

Macular degeneration is the most common cause of vision loss and blindness in individuals over the age of fifty. About 1.8 million US residents currently have advanced age-related macular degeneration, so it's important to have your eyes examined regularly by your eye care professional.

Here are some treatment options for Dry and Wet Age Related Macular Degeneration.

Nutritional supplements and Dry Age Related Macular Degeneration (AMD)

The Age-Related Eye Disease Study 2 (AREDS2) showed that people at high risk of developing advanced stages of AMD benefited from taking dietary supplements. Supplements lowered the risk of macular degeneration progression by 25 percent. These supplements did not benefit people with early AMD or people without AMD.

Following is the supplementation:

  • Vitamin C - 500 mg
  • Vitamin E - 400 IU
  • Lutein – 10 mg
  • Zeaxanthin – 2 mg
  • Zinc Oxide – 80 mg
  • Copper – 2 mg (to prevent copper deficiency that may be associated with taking high amount of zinc)

Another study showed a benefit in eating dark leafy greens and yellow, orange and other fruits and vegetables. These vitamins and minerals listed above are recommended in addition to a healthy, balanced diet.

It is important to remember that vitamin supplements are not a cure for AMD, nor will they restore vision. However, these supplements may help some people maintain their vision or slow the progression of the disease.

Wet AMD treatments

The most common treatment for wet AMD is an eye injection of anti-vascular endothelial growth factor (anti-VEGF). This treatment blocks the growth of abnormal blood vessels, slows their leakage of fluid, may help slow vision loss, and in some cases can improve vision. There are currently three anti-VEGF drugs available: Avastin, Lucentis, and Eylea.

You may need monthly injections for a prolonged period of time for treatment of wet AMD.

Laser Treatment for Wet AMD

Some cases of wet AMD may benefit from thermal laser. This laser destroys the abnormal blood vessels in the eye to prevent leakage and bleeding in the retina. A scar forms where the laser is applied and may cause a blind spot that might be noticeable in your field of vision.

Photodynamic Therapy or PDT

Some patients with wet AMD might benefit from photodynamic therapy (PDT). A medication called Visudyne is injected into your arm and the drug is activated as it passes through the retina by shining a low-energy laser beam into your eye. Once the drug is activated by the light it produces a chemical reaction that destroys abnormal blood vessels in the retina. Sometimes a combination of laser treatments and injections of anti-VEGF mediations are employed to treat wet AMD.


Article contributed by Jane Pan M.D.

The content of this blog cannot be reproduced or duplicated without the express written consent of Eye IQ

The jury is still out on that question. There is some supportive experimental data in animal models but no well-done human studies that show any significant benefit.

What you shouldn’t do is pass up taking the AREDS 2 nutritional supplement formula, which is clinically proven to reduce the risk of severe visual loss in. Almost all the data supporting the POSSIBLE benefits of bilberry in visual conditions is related to NON-HUMANS. Stick with the AREDS 2 formula that has excellent clinical evidence.

So, what is bilberry and why do some people use it?

Bilberry (Vaccinium myrtillus), a low-growing shrub that produces a blue-colored berry, is native to Northern Europe and grows in North America and Asia. It is naturally rich in anthocyanins, which have anti-oxidant properties.

During World War II, British pilots in the Royal Air Force ate bilberry jam, hoping to improve their night vision. No one is exactly sure where the impetus to do this came from, but it is believed that this event is what lead to some widespread claims that bilberry was good for your eyes.

A study by JH Kramer,  Anthocyanosides of Vaccinium myrtillus (Bilberry) for Night Vision - A Systematic Review of Placebo-Controlled Trials, reviewed most of the literature pertaining to the claim that bilberry improves night vision. He found that the four most recent trials, which were all rigorous randomized controlled trials (RCTs), showed no correlation with bilberry extract and improved night vision. A fifth RCT and seven non-randomized controlled trials reported positive effects on outcome measures relevant to night vision, but these studies had less-rigorous methodology.

Healthy subjects with normal or above-average eyesight were tested in 11 of the 12 trials. The hypothesis that V. myrtillus improves normal night vision is not supported by evidence from rigorous clinical studies. There is a complete absence of rigorous research into the effects of the extract on subjects suffering impaired night vision due to pathological eye conditions.

Even though there is no solid evidence in human studies that bilberry produces any positive visual effects on night vision there is some experimental evidence that implies it might be useful in some ocular conditions whose mode of action is oxidative stress. There are recent epidemiologic, molecular and genetic studies that show a major role of oxidative stress in age-related macular degeneration.

There have been some studies showing oxidative protective effects of bilberry in non-human models. 

In Protective effects of bilberry and lingonberry extracts against blue-light emitting diode light-induced retinal photoreceptor cell damage in vitro, Ogawa et al showed in cultured mouse cells that adding bilberry extract to cells before subjecting them to high-energy short-wavelength light that the cells survived better mostly by reducing the amount of reactive oxidative molecules. 

In Retinoprotective Effects of Bilberry Anthocyanins via Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Mechanisms in a Visible Light-Induced Retinal Degeneration Model in Pigmented Rabbits, Wang et al found similarly improved survival of pigmented rabbit retinal cells when exposed to bilberry abstract prior to high-intensity light.

But bilberry is not without potential side effects.

Bilberry possesses anti-platelet activity; it may interact with NSAIDs, particularly aspirin. And excessive drinking of bilberry juice may cause diarrhea. One study of 2,295 people given bilberry extract found a 4% incidence of side effects or adverse events. Further, bilberry side effects may include mild digestive distress, skin rashes and drowsiness. Chronic uses of the bilberry leaf may lead to serious side effects. High doses of bilberry leaf can be poisonous.

Bilberry has not been evaluated by the Food and Drug Administration for safety, effectiveness, or purity.


Article contributed by Dr. Brian Wnorowski, M.D.

The retina is the nerve tissue that lines the inside back wall of your eye. Light travels through the pupil and lens and is focused on the retina, where it is converted into a neural impulse and transmitted to the brain. If there is a break in the retina, fluid can track underneath the retina and separate it from the eye wall. Depending on the location and degree of retinal detachment, there can be very serious vision loss.


The three 3 F’s are the most common symptoms of a retinal detachment:

  • Flashes: Flashing lights that are usually seen in peripheral (side) vision.

  • Floaters: Hundreds of dark spots that persist in the center of vision.

  • Field cut: Curtain or shadow that usually starts in peripheral vision that may move to involve the center of vision.


Retinal detachments can be broadly divided into three categories depending on the cause of the detachment:

Rhegmatogenous retinal detachments: Rhegmatogenous means “arising from a rupture,” so these detachments are due to a break in the retina that allows fluid to collect underneath the retina. A retinal tear can develop when the vitreous (the gel-like substance that fills the back cavity of the eye) separates from the retina as part of the normal aging process.

The risk factors associated with this type of retinal detachment:

  • Lattice degeneration – thinning of the retina.

  • High myopia (nearsighted) - can result in thinning of the retina.

  • History of a previous retinal break or detachment in the other eye.

  • Trauma.

  • Family history of retinal detachment.

Tractional retinal detachments: These are caused by scar tissue that grows on the surface of the retina and contraction of the scar tissue pulls the retina off the back of the eye. The most common cause of scar tissue formation is due to uncontrolled diabetes.

Exudative retinal detachments: These types of detachments form when fluid accumulates underneath the retina. This is due to inflammation inside the eye that results in leaking blood vessels. The visual changes can vary depending on your head position because the fluid will shift as you move your head. There is no associated retinal hole or break in this type detachment. Of the three types of retinal detachments, exudative is the least common.

Diagnostic tests

  • A dilated eye exam is needed to examine the retina and the periphery. This may entail a scleral depression exam where gentle pressure is applied to the eye to examine the peripheral retina.

  • A scan of the retina (optical coherence tomography) may be performed to detect any subtle fluid that may accumulate under the retina.

  • If there is significant blood or a clear view of the retina is not possible then an ultrasound of the eye may be performed.


The goal of treatment is to re-attach the retina to the eye wall and treat the retinal tears or holes.

In general, there are four treatment options:

  • Laser: A small retinal detachment can be walled off with a barrier laser to prevent further spread of the fluid and the retinal detachment.

  • Pneumatic Retinopexy: This is an office-based procedure that requires injecting a gas bubble inside the eye. After this procedure, you need to position your head in a certain direction for the gas bubble to reposition the retina back along the inside wall of the eye. A freezing or laser procedure is performed around the retinal break. This procedure has about 70% to 80% success rate but not everyone is a good candidate for a pneumatic retinopexy.

  • Scleral buckle: This is a surgery that needs to be performed in the operating room. This procedure involves placing a silicone band around the outside of the eye to bring the eye wall closer to the retina. The retinal tear is then treated with a freezing procedure. Vitrectomy: In this surgery, the vitreous inside the eye is removed and the fluid underneath the retina is drained. The retinal tear is then treated with either a laser or freezing procedure. At the completion of the surgery, a gas bubble fills the eye to hold the retina in place. The gas bubble will slowly dissipate over several weeks. Sometimes a scleral buckle is combined with a vitrectomy surgery.


Final vision after retinal detachment repair is usually dependent on whether the macula (central part of the retina that you use for fine vision) is involved. If the macula is detached, then there is usually some decrease in final vision after reattachment. Therefore, a good predictor is initial presenting vision. We recommend that patients with symptoms of retinal detachments (flashes, floaters, or field cuts) have a dilated eye exam. The sooner the diagnosis is made, the better the treatment outcome.


Article contributed by Dr. Jane Pan

This blog provides general information and discussion about eye health and related subjects. The words and other content provided in this blog, and in any linked materials, are not intended and should not be construed as medical advice. If the reader or any other person has a medical concern, he or she should consult with an appropriately licensed physician. The content of this blog cannot be reproduced or duplicated without the express written consent of Eye IQ.

There are several different variations of Glaucoma, but in this article we will mainly focus on Primary Open Angle Glaucoma. This means that there is no specific underlying cause for the Glaucoma like inflammation, trauma or a severe cataract. It also means that the drainage angle where fluid is drained from the inside of the eye into the bloodstream is not narrow or closed.

Closed or Narrow Angle Glaucoma, which will be discussed in another article, is treated differently from Open Angle Glaucoma

In the U.S., Primary Open Angle Glaucoma (POAG) is by far the most common type of Glaucoma we treat.

Glaucoma is a disease where the Optic Nerve in the back of the eye deteriorates over time, and that deterioration has a relationship to the Intraocular Pressure (IOP).  Most - but not all - people diagnosed with Glaucoma have an elevated IOP.  Some people have fairly normal IOP’s but show the characteristic deterioration in the Optic Nerve. Regardless of whether or not the pressure was high initially, our primary treatment is to lower the IOP. We usually are looking to try to get the IOP down by about 25% from the pre-treatment levels.

The two mainstays of initial treatment for POAG in the U.S. are medications or laser treatments. There are other places in the world where Glaucoma is initially treated with surgery. However, while surgery can often lower the pressure to a greater degree than either medications or laser treatments, it comes with a higher rate of complications. Most U.S. eye doctors elect to go with the more conservative approach and utilize either medications - most often in the form of eye drops - or a laser treatment.


There are several different classes of medications used to treat Glaucoma.

The most common class used are the Prostaglandin Analogues or PGA’s.  The PGA’s available in the U.S. are Xalatan (latanaprost), Travatan (travapost), Lumigan (bimatoprost) and Zioptan (tafluprost).

PGA’s are most doctors’ first line of treatment because they generally lower the IOP better than the other classes; they are reasonably well tolerated by most people; and they are dosed just once a day, while most of the other drugs available have to be used multiple times a day.

The other classes of drugs include beta-blockers that are used once or twice a day; carbonic anhydrase inhibitors (CAI’s ), which come in either a drop or pill form and are used either twice or three times a day; alpha agonists that are used either twice or three times a day; and miotics, which are used three or four times a day. All of these other medications are typically used as either second-line or adjunctive treatment when the PGA’s are not successful in keeping the pressure down as single agents.

There are also several combination drops available in the U.S. that combine two of the second-line agents (Cosopt, Combigan, and Symbrinza).


The second option as initial treatment is a laser procedure.

The two most common laser treatments for Open Angle Glaucoma are Argon Laser Trabeculoplasty (ALT) or Selective Laser Trabeculoplasty (SLT).  These treatments try and get an area inside the eye called the Trabecular Meshwork - where fluid is drained from the inside of the eye into the venous system - to drain more efficiently.

These treatments tend to lower the pressure to about the same degree as the PGA’s do with over 80% of patients achieving a significant decrease in their eye pressure that lasts at least a year.  Both laser treatments can be repeated if the pressure begins to rise again in the future but the SLT works slightly better as a repeat procedure compared to the ALT.

Article contributed by Dr. Brian Wnorowski, M.D.

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