Dr. Jeff Hersh: How does an eye stroke differ from others?

Dr. Jeff Hersh

Q: My father had an eye stroke in his right eye and has lost his vision. How does this differ from the usual kind of stroke?

A: It sounds like your dad had central retinal artery occlusion, sometimes called an eye stroke.

The central retinal artery supplies blood to the retina. The retina is the picture screen behind the lens of the eye where the rods and cones that receive light transmit the information via the optic nerve to the brain. The CRA also supplies blood to the optic nerve. This artery is pretty thin, typically 100-200 microns in diameter (0.04 to 0.08 inches). To put this in perspective, a red blood cell is about 7 microns in diameter.

Interestingly, the sharpest vision comes from a special area of the retina with the highest density of rods and cones called the fovea, and its blood supply is from a different artery.

In analogy to an ischemic brain stroke - where the blood supply to part of the brain is blocked - obstruction of the CRA compromises blood supply to the optic nerve and most of the retina. If this persists for approximately 1 1/2 hours or longer, there may be cell damage and permanent vision loss.

There are two main ways the CRA becomes obstructed. Small particles (emboli) can block it. For example, plaque can break away from a diseased artery in the neck or a blood clot can come from the heart of a patient with an irregular heart beat (atrial fibrillation). These same mechanisms can lead to a brain stroke, with risk factors of high cholesterol, high blood pressure, diabetes mellitus, smoking, atrial fibrillation, older age, etc.

The other common way the CRA may become blocked is from becoming inflamed to the point where blood cannot pass through it. This most commonly happens from giant cell (temporal) arteritis, which is responsible for 5 percent to 10 percent of all cases of CRAO.

When the CRA becomes blocked, the result is acute painless loss of vision in the affected eye. The diagnosis of CRAO is made based on this history as well as examination of the eye, which shows a milky white retina with a cherry red spot (where the fovea is still receiving adequate blood) in the center.

Overall, CRAO is a rare condition, affecting 1 to 10 people per 100,000.

Testing to determine the cause of the CRAO may include blood tests (to screen for temporal arteritis), ECG (to check for atrial fibrillation), as well as others.

Early intervention to try to unblock the CRA can prevent long-term vision loss. Appropriate massage of the eye by a medical professional to dislodge a presumed emboli (although no studies have been done proving the effectiveness of this technique), clot busting medications or other interventions (such as draining fluid from the eye) may be considered. Since embolic causes of CRAO share risk factors with stroke and heart disease, treatment to minimize these risks is indicated even if it is too late to prevent vision loss.

Temporal arteritis is treated with steroid medications to decrease the inflammation. This is true even if permanent vision loss has occurred in the initially affected eye in order to prevent problems in the other eye.

Only about 25 percent of patients retain useful vision after CRAO. Since early treatment and less vision loss at presentation indicate a better prognosis, anyone experiencing acute vision loss should seek immediate medical care. Embolic causes of CRAO are indeed "eye strokes," and just like other strokes these require immediate evaluation and early intervention to improve outcomes.

Jeff Hersh, Ph.D., M.D., F.A.A.P., F.A.C.P., F.A.A.E.P., can be reached at DrHersh@juno.com.