What Is an Eye Stroke?

Vision loss due to the restriction of blood flow in the eye

Man getting an eye exam

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An eye stroke is a term used to describe the loss of vision caused by reduced flow of blood to the eye. There are different conditions associated with eye stroke, some that affect the retina (the layer of tissue at the back of the eye that converts light images into nerve signals) and others thst damage the optic nerve (which carries nerve signals to the brain).

Symptoms of eye stroke include sudden blurring or vision loss in all or part of one eye, usually without pain. While the sudden loss of vision can be frightening, prompt medical attention can often prevent or limit permanent damage.

Types of Eye Stroke

Eye strokes are caused by occlusion (blockage) of a blood vessel that services the back of the eye. The causes of eye stroke differ by the mechanism of the blockage, the type of blood vessel affected, and the part of the eye serviced by the vessel.

The four common most common causes of eye strokes are:

  • Retinal artery occlusion (RAO): One or more arteries carrying oxygen to the retina are blocked.
  • Retinal vein occlusion (RVO): The small veins carrying oxygen away from the retina are blocked.
  • Arteritic anterior ischemic optic neuropathy (AAION): There is loss of blood flow to the optic nerve, mainly involving the medium-to-large blood vessels and most often due to an inflammatory disorder known as giant cell arteritis (GCA).
  • Non-arteritic anterior ischemic optic neuropathy (NAION): There is oss of blood flow to the optic nerve, mainly involving the smaller vessels and without inflammation.

Retinal occlusion and ischemic optic neuropathy can sometimes co-occur.

The term arteritic describes reduced blood flow that occurs with inflammation, while non-arteritic describes reduced blood flow without inflammation.

Eye Stroke Symptoms

Eye stroke usually occurs with little-to-no warning of the impending vision loss. Most people with eye stroke notice a loss of vision in one eye upon waking in the morning or experience worsening vision over the course of hours or days. There is rarely any pain.

Some people will notice darkened areas (blind spots) in either the upper or lower half of the field of vision. There may also be a loss of peripheral vision ("tunnel vision") or visual contrast, as well as light sensitivity.

Retinal Vascular Occlusion

Depending on which vessels in the eye are occluded, the symptoms and severity of the resulting visual disturbance can vary. The types of retinal occlusion are broadly characterized as follows:

  • Central retinal artery occlusion (CRAO): Involving the primary artery that delivers oxygenated blood to the retina, this usually manifests with sudden, profound vision loss in one eye with no pain.
  • Central retinal vein occlusion (CRVO): Involving the primary vein that receives deoxygenated blood from the retina, this can cause sudden, painless vision loss ranging from mild to severe.
  • Branch retinal artery occlusion (BRAO): Involving smaller vessels that branch off of the central retinal artery, this can manifest with the loss of peripheral vision and/or loss in parts of the central vision.
  • Branch retinal vein occlusion (BRVO): Involving smaller vessels that branch off of the central retinal vein, this can cause reduced vision, peripheral vision loss, distorted vision, or blind spots.

Ischemic Optical Neuropathy

The symptoms of anterior ischemic optical neuropathy can vary depending on whether the condition is arteritic (AAOIN) or non-arteritic (NAOIN). The symptoms are categorized as follows:

  • AAOIN: Occurring secondary to giant-cell arteritis, it can result in the complete loss of vision in one eye, often within hours. If left untreated, AAOIN may affect the other eye in one to two weeks. Vision loss may be accompanied by other symptoms of GCA, including fever, fatigue, jaw spasms, scalp tenderness, muscle aches, and unintentional weight loss.
  • NAOIN: This usually manifests with painless vision loss over the course of several hours or day ranging from mild blurring to total blindness in the affected eye. In many cases, there will be vision loss in the lower part of the visual field. Color vision may also be reduced in tandem with the severity of the vision loss.

Causes

Eye stroke is caused when the flow of blood to the back of the eye is impaired, starving tissues of oxygen. In the same way a stroke causes cell death in the brain due to the lack of oxygen, eye stroke can destroy tissues of the retina or optic nerve, thus preventing transmission of nerve signals to the brain. The causes and risk factors of eye stroke vary by the condition involved.

Retinal Vascular Occlusion

RAO and RVO are caused by physical obstruction of the retinal artery or retinal vein, respectively. This may be due to a blood clot (thromboembolus) or a small piece of cholesterol (plaque) that has broken off the wall of a blood vessel.

The occlusion may last for a few seconds or minutes if the obstruction breaks up. If it doesn't self-destruct, the obstruction may be permanent.

Both RAO and RVO are closely linked to cardiovascular diseases (involving the heart and blood vessels) and cerebrovascular diseases (involving the blood vessels of the brain). The risk factors for retinal vascular occlusion include:

Retinal occlusion tends to affect people over 50, with men being slightly more at risk than women. Retinal occlusion in younger people often is related to a blood clotting disorder such as thrombophilia.

Glaucoma also is a risk factor for retinal occlusion, although it occurs far more frequently with RVO than RAO. Studies suggest people with glaucoma are five times more likely to develop CRVO than the general population.

Ischemic Optical Neuropathy

AAION and NAION are less understood causes of eye stroke. While AAION is almost always the result of giant cell arteritis (GCA), the cause for GCA remains unknown. Similarly, with NAOIN, the vascular damage to the optic nerve appears related to a multitude of factors that uncommonly come together to cause nerve injury.

AAION

AAION is almost exclusively caused by GCA, also known at temporal arteritis. GCA is a form of vasculitis (blood vessel inflammation) that mainly affects the arteries around the head and neck but can extend to the chest.

Other rare causes of AAION are lupus (an autoimmune disorder) and periarteritis nodosa (a rare inflammatory blood vessel disease).

GCA causes inflammation of the medium to large blood vessels which can "spill over" to the smaller vessels, causing them to swell and obstruct blood flow. When the vessels servicing the optic nerve are affected, AAION can result.

GCA is believed to have both genetic and environmental origins. There are several known triggers for GCA in people who've inherited a predisposition to the condition. One is a severe bacterial or viral infection: Studies suggest varicella-zoster virus (shingles) may be involved in the onset of GCA in up to 74% of people.

Another is inflammatory disorders (including autoimmune diseases). For example, GCA is closely linked to polymyalgia rheumatica, which occurs in 40% to 50% of people with GCA. High-dose antibiotics also have been implicated.

GCA affects around two of every 100,000 people in the United States each year, mainly those of Nordic origin over 50. Women are up to three times more likely to have GCA—and thereby AAION—than men.

NAION

NAION is caused by the transient disruption of blood flow to the optic nerve unrelated to inflammation. The disruption can be caused by a multitude of co-occurring factors that either slow the flow of blood to the optic nerve (hypoperfusion) or stop it altogether (nonperfusion). Unlike AAION, NAION mainly affects the smaller vessels.

One condition believed to increase the risk of NAION is nocturnal hypotension (low blood pressure during sleep) which can reduce the amount of blood that reaches the optic nerve.

The decreased blood circulation, hypovolemia, causes progressive injury as some, but not enough, blood reaches the optic nerve. Because of this, vision loss with NAION tend to be less abrupt than with AAION.

Studies suggest at least 73% of people with NAION are affected by nocturnal hypotension.

Another common cause of hypotension and hypovolemia is end-stage kidney disease. People with end-stage kidney disease are at three times greater risk of NAION than people in the general population.

With that said, having hypotension or hypovolemia does not mean developing NAION is inevitable. Other risk factors are believed to contribute.

One is the shape of the optic disc, a circular area on the back of the eye that connects the retina to the optic nerve. Optic discs normally have an indentation in the center called a cup. Small to nonexistent cups are considered strong risk factors for NAION, as is high intraocular pressure commonly experienced by people with glaucoma.

On rare occasions, NAION may be the result of a blood clot or other obstruction affecting a vessel servicing the optic nerve. When this occurs, it is not uncommon for NAION to be accompanied by RAO or RVO.

NAION affects 10 of every 100,000 Americans each year, almost exclusively those over 50. Whites are affected more than non-whites, while men are nearly twice as likely to have NAION as women

Diagnosis

If your ophthalmologist suspects you may have had an eye stroke, they will conduct a routine exam first by checking your vision, evaluating your eye pressure, and examining your retina.

Based on the results and the characteristics of your vision loss, along with a review of your medical history and risk factors, the ophthalmologist may perform some or all of the following tests, which are usually effective in diagnosing retinal vascular occlusion:

  • Ophthalmoscopy: An examination of the interior structure of the eye lighted magnifying device called an ophthalmoscope
  • Non-contact tonometry (NCT): Also known as an air puff test—a non-invasive procedure that measures intraocular eye pressure and can help diagnose glaucoma
  • Optical coherence tomography (OCT): A non-invasive imaging study that uses light waves to scan the retina and capture highly detailed images
  • Fluorescein angiography: A procedure in which a fluorescent dye injected into a vein in the arm will flow to the vascular structure of the eye to highlight it

Other tests may be ordered to identify the underlying cause of eye stroke. Among them, blood pressure readings and blood tests (including serum glucose, complete blood count, platelet count, and erythrocyte sedimentation rate) can help identify if diabetes, cardiovascular disease, a clotting disorder, or an inflammatory process is involved.

Diagnosing Ischemic Optical Neuropathy

Because retinal occlusions involve the physical obstruction of a blood vessel, they are often easier—or at least more straightforward—to diagnose than ischemic optical neuropathy.

While ophthalmoscopy, OCT, and fluorescein angiography can help detect optic nerve damage, AAION or NAION requires an extensive investigation with additional tests and procedures.

AAION

AAION is suspected if the erythrocyte sedimentation rate (ESR) is above 70 millimeters per minute (mm/min) along with an elevated C-reactive protein (CRP) test. Both tests measure systemic inflammation.

There will also be characteristic signs of GCA, including jaw spasm, fever, muscle aches, and scalp tenderness.

An imaging test called magnetic resonance imaging (MRI) can help differentiate AAION from NAION. With AAION, the MRI will reveal a "central bright spot" on the optic nerve which is characteristic of giant-cell arteritis.

To confirm GCA as the cause, the ophthalmologist will order a biopsy of the temporal artery. Performed under local anesthesia on an outpatient basis, the biopsy is used to obtain a small sample of tissue from the temporal artery which is situated close to the skin just in front of the ears and continues to the scalp.

A temporal artery biopsy is considered the gold standard for diagnosing of giant-cell arteritis. The thickening and fragmentation of arterial tissues paired with an infiltration of inflammatory cells are confirmatory of the disease.

NAION

NAION occurs without inflammation, so there will be no elevation of the ESR or CRP. One clue that NAION is involved is the minimal-to-no cupping of the optic nerve. This can be detected using OCT or the combination of fluorescein angiography with a color doppler ultrasound (which uses sound waves to image tissues).

Another telling sign of NAION is a relative afferent pupil defect (RAPD) in which the pupil of the unaffected eye responds differently to light than the affected eye. This can help differentiate NAION from other forms of optical neuropathy, which may be neurologic rather than vascular in nature.

To confirm a NAION diagnosis, the ophthalmologist will exclude other possible causes in the differential diagnosis, including:

NAION is diagnosed clinically based on a review of symptoms, optic nerve characteristics, and predisposing risk factors. There are no tests to confirm NAION.

Treatment

The goal of treatment for the various types of eye stroke is to restore vision or at the very least minimize vision loss.

Retinal Vascular Occlusion

Many people with RAO and RVO will regain vision without treatment, although it rarely returns fully to normal. Once a blockage has occurred, there is no way to physically unblock it or dissolve the embolus.

To improve blood flow to the retina, doctors may inject a corticosteroid drug such as triamcinolone acetonide into the eye to help relax adjacent blood vessels and reduce swelling caused by inflammation. Severe cases may benefit from an implant of a corticosteroid drug called dexamethasone which comes as a pellet that is injected near the site of the occlusion.

To reduce the risk of occlusion in the unaffected eye, doctors will often recommend aspirin or another blood thinner such as warfarin. If the occlusion was caused by a dislodged piece of plaque from an arterial wall, antihypertensive or cholesterol-lowering drugs may be prescribed.

There is also an experimental treatment gaining popularity among ophthalmologists called anti-vascular endothelial growth factor (anti-VEGF). Anti-VEGF is a monoclonal antibody injected into the eye that blocks the growth of new blood vessels that can lead to glaucoma and progressive vision loss.

Eylea (aflibercept) and Lucentis (ranibizumab) are two anti-VEGF drugs approved by the U.S. Food and Drug Administration.

Eylea and Lucentis are approved to treat macular degeneration but are sometimes used off-label to prevent progressive vision loss in people with RAO or RVO.

AAION

This condition requires aggressive treatment to prevent total blindness in the affected eye. Once vision loss occurs, it is almost never fully reversible. Without treatment, vision loss will occur in the majority of people with AAION and eventually affect the other eye in 50% of cases.

The first line of treatment is systemic corticosteroids delivered either orally (in tablet form) and or intravenously (injected into a vein). Oral prednisone is most often used in mild to moderate cases. It's taken daily for several weeks or months and then gradually tapered off to prevent withdrawal and other serious side effects.

Severe AAION may require intravenous methylprednisolone for the first three days, followed by a daily course of oral prednisone.

Some doctors, concerned about the long-term side effects of prednisone use (including the risk of cataracts), may opt to taper the corticosteroid dose while adding the immunosuppressive drug methotrexate to the treatment plan.

Once prednisone is stopped, methotrexate can continue as a maintenance drug. Studies have shown that methotrexate, taken by mouth once weekly, is effective in preventing the relapse of GCA.

Actrema (tocilizumab) is another drug used in "corticosteroid-sparing" therapies. It is an injectable monoclonal antibody approved for the treatment of GCA that is typically used when prednisone underperforms or poses a risk of severe side effects.

As with methotrexate, Actrema is given once weekly and introduced to the treatment plan as the prednisone dose is gradually tapered down.

NAION

NAION can be as challenging to treat as it is to diagnose, but if not treated, it causes visual loss or impairment in 45% of people.

As with AAION, corticosteroid drugs are used in first-line therapy to improve blood flow to the optic nerve. When delivered at high doses, oral prednisone can improve vision in 85% of people with AAION, although the field of vision will often remain impaired.

Though corticosteroid eye injections have been proposed as a treatment for AAION, they have not proven to be any more effective than oral corticosteroids and may end up injuring the optic nerve. Anti-VGF monoclonal antibodies have also not proven to be effective in treating NAION.

To prevent recurrence or the involvement of the other eye, the precipitating cause of hypotension or hypovolemia must be treated. Unless an occlusion is involved, aspirin, blood thinners, or antiplatelet drugs are of little use in treating NAION or preventing involvement of the other eyes.

One approach sometimes considered for people with severe NAION is optic nerve sheath decompression (OPSD). OPSD is a surgical procedure used to alleviate pressure on the optic nerve, thereby improving the transmission of nerve signals to the brain.

OPSD is primarily used to treat vision loss caused by high intracranial pressure (such as can occur with meningitis and solid brain tumors).

Optic nerve sheath decompression may be useful in people with acute NAION symptoms, potentially stopping the progression of vision loss, but is usually not helpful when damage to the optic nerve has already occurred.

A Word From Verywell

If you experience sudden vision loss of any sort, see your doctor immediately or go to your nearest emergency room. Prompt treatment—delivered within hours, not days—is essential to preventing vision loss, particularly if GCA is involved.

If you notice a vision change that is progressive or unexplained, that is usually enough to warrant a visit to your doctor or an ophthalmologist. Never ignore changes in vision, however minimal.

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