Amaurosis fugax is a medical term describing a sudden, temporary loss of sight in one eye. It is also known as Transient Monocular Blindness (TMB). The vision loss occurs due to a brief disruption in the blood flow to the retina, the light-sensitive tissue at the back of the eye. Amaurosis fugax is a symptom of an underlying health problem, not a disease itself, and signals a temporary event requiring immediate investigation.
Defining the Transient Event
The patient’s experience of amaurosis fugax is distinct. The loss of vision is usually painless and occurs suddenly in one eye. Many people describe the sensation as a curtain or shade being pulled down over their field of view, often starting from the top and progressing downward, or sometimes moving from the side.
The fleeting nature of the event defines the condition, with sight loss usually lasting from a few seconds to several minutes. Episodes rarely persist for more than 30 minutes, and if vision loss lasts for hours, it is generally no longer classified as amaurosis fugax. Full, normal sight returns spontaneously once the episode concludes.
Though the visual disturbance is brief, it represents a temporary lack of oxygen supply to the retina, known as transient retinal ischemia. This temporary ischemic event is similar in mechanism to a transient ischemic attack (TIA) in the brain, where symptoms resolve quickly. The rapid, complete recovery of vision is the signature feature differentiating this event from more permanent forms of blindness.
Identifying the Systemic Vascular Causes
The underlying cause of amaurosis fugax is often an embolic event, where a small particle travels through the bloodstream and temporarily blocks an artery supplying the retina. The most common source for these particles is the carotid artery in the neck, the main vessel supplying blood to the head and eyes. Atherosclerosis, characterized by plaque buildup on artery walls, can lead to carotid artery stenosis, or narrowing of the vessel.
Small fragments of this atherosclerotic plaque, composed of cholesterol and fat, can break off and travel up the internal carotid artery toward the eye. When one of these microemboli lodges in the central retinal artery, it momentarily starves the retina of blood, causing vision loss. The embolus then passes through or dissolves, allowing blood flow to resume and sight to return.
Clots originating from the heart are another significant cause, especially in patients with atrial fibrillation or other cardiac abnormalities. An irregular heartbeat allows blood to pool and clot inside the heart, and these clots can travel to the eye’s circulation. Amaurosis fugax is a serious warning sign, as the same embolic mechanism affecting the eye can also affect the brain, increasing the risk of a permanent stroke.
Less common causes include vasospasm, which is a temporary narrowing of the blood vessel due to muscle contraction, or hypercoagulable states, where the blood has an increased tendency to clot. Inflammation of the blood vessels, such as in giant cell arteritis, can also compromise blood flow to the optic nerve and retina, presenting with similar transient vision loss, especially in older adults.
Immediate Medical Response and Treatment Pathways
Amaurosis fugax is a medical emergency requiring immediate evaluation, even if vision has completely returned. Prompt assessment is necessary because the transient vision loss indicates a high risk for a more permanent event, such as a stroke. Patients should seek emergency medical attention immediately to begin the diagnostic workup.
The diagnostic process focuses on identifying the source of the temporary blockage. A physical examination is performed alongside laboratory studies, including blood tests for cholesterol, blood sugar, and inflammatory markers like C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). These markers are important for patients over 50 to rule out giant cell arteritis. A carotid duplex ultrasound is a standard imaging test used to visualize the carotid arteries and measure the degree of any narrowing.
To check for a cardiac source, an electrocardiogram (EKG) is performed to detect heart rhythm irregularities like atrial fibrillation. Depending on the initial findings, a computed tomography (CT) or magnetic resonance imaging (MRI) scan of the brain may be ordered. These imaging studies check for signs of a previous, silent stroke and guide the subsequent treatment strategy.
Treatment pathways are determined by the underlying cause identified during the evaluation. For nearly all patients, optimal medical therapy is initiated, which includes anti-platelet medications like aspirin and often a short course of dual anti-platelet therapy, such as aspirin combined with clopidogrel. High-intensity statin drugs are also prescribed to lower LDL cholesterol levels and stabilize existing plaques.
If severe carotid artery stenosis (70% or more narrowing) is found, a surgical procedure called carotid endarterectomy, which removes the plaque, or carotid artery stenting may be recommended to reduce stroke risk. If the cause is determined to be from the heart, such as a clot due to atrial fibrillation, anticoagulation medication may be prescribed. The goal of all treatment is to manage systemic risk factors like high blood pressure and diabetes to prevent future vascular events.