What is the pathophysiology of amaurosis fugax (transient monocular vision loss)?

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From the Guidelines

Amaurosis fugax is a transient monocular blindness caused by temporary reduction of blood flow to an eye, most commonly due to atherosclerosis of the ipsilateral internal carotid artery, with embolism from the carotid artery or heart being a key mechanism. The pathophysiology of amaurosis fugax involves a sudden loss of vision, often described as a shade drawn upward or downward over the field of view, resulting from temporary blockage of the ophthalmic artery by emboli such as fibrin, cholesterol crystals (Hollenhorst plaques), fat, or material arising from fibrocalcific degeneration of the aortic or mitral valves 1.

Key Causes and Mechanisms

  • Carotid artery stenosis or occlusion
  • Atherosclerosis
  • Dissection
  • Arteritis
  • Radiation-induced arteriopathy
  • Arterial embolism
  • Cardiogenic embolism
  • Atheroembolism
  • Hypotension
  • Intracranial hypertension
  • Glaucoma
  • Migraine
  • Vasospastic or occlusive disease of the ophthalmic artery

The risk of stroke in patients with amaurosis fugax is significant and is related to the number of stroke risk factors, with a 3-year risk of stroke with medical treatment alone being 1.8% in those with 0 or 1 risk factor, 12.3% in those with 2 risk factors, and 24.2% in those with 3 or 4 risk factors 1. Prompt evaluation and management of amaurosis fugax are crucial to prevent subsequent cerebrovascular events and potential permanent blindness in the affected eye.

From the Research

Pathophysiology of Amaurosis Fugax

The pathophysiology of amaurosis fugax is closely related to carotid artery disease, particularly carotid stenosis and ulcerated plaque.

  • Carotid artery stenosis is a significant risk factor for amaurosis fugax, with studies showing a high correlation between the two 2, 3.
  • Ulcerated plaque is also a major contributor to the development of amaurosis fugax, with one study finding a high correlation (0.87) between ulcerated plaque and amaurosis fugax 2.
  • The presence of risk factors such as hypertension, diabetes, coronary artery disease, tobacco, and hyperlipidemia also increases the likelihood of developing amaurosis fugax 2, 4.

Carotid Plaque Morphology

The morphology of carotid plaques plays a crucial role in the development of amaurosis fugax.

  • Heterogeneous, complex carotid plaques are more likely to cause amaurosis fugax, with studies showing a correlation between these types of plaques and the development of the condition 3.
  • The classification of carotid atheromata plaques into three groups (hemorrhagic plaque, dystrophic calcification, and ulcerated plaque) has helped to identify the types of plaques most likely to cause amaurosis fugax 2.

Clinical and Doppler Findings

Clinical, Doppler, and angiographic findings are essential in diagnosing and managing amaurosis fugax.

  • Atherosclerotic lesions are commonly detected on Doppler or angiographic examination in patients with amaurosis fugax, with one study finding lesions in 63% of patients 5.
  • Patient age is a significant factor in predicting the presence of relevant carotid occlusive disease, with all lesions found in patients over 50 years of age 5.
  • Carotid ultrasound is a useful tool in diagnosing and managing amaurosis fugax, with studies showing a high prevalence of significant carotid stenosis in patients with the condition 4.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Amaurosis fugax: the importance of carotid plaque morphology.

Australian and New Zealand journal of ophthalmology, 1988

Research

Amaurosis fugax: risk factors and prevalence of significant carotid stenosis.

Clinical ophthalmology (Auckland, N.Z.), 2016

Research

Amaurosis fugax: clinical, Doppler and angiographic findings.

Acta neurologica Scandinavica, 1988

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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