Amaurosis fugax pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Prior to 1990, amaurosis fugax could, "clinically, be divided into four identifiable symptom complexes, each with its underlying pathoetiology: embolic, hypoperfusion, angiospasm, and unknown."[1] In 1990, the causes of amaurosis fugax were better refined by Amaurosis Fugax Study Group, which has defined five distinct causes of transient monocular blindness: embolic, hemodynamic, ocular, neurologic, and idiopathic.[2] Concerning the pathology underlying these causes (stay idiopathic), "some of the more frequent causes include atheromatous disease of the internal carotid or ophthalmic artery, vasospasm, optic neuropathy, giant cell arteritis, angle-closure glaucoma, increased intracranial pressure, orbital compressive disease, a steal phenomenon, and blood hyperviscosity or hypercoagulability."[3]

Pathophysiology

Embolic and Hemodynamic Origin

With respect to embolic and hemodynamic causes, this transient monocular visual loss ultimately occurs due to a temporary reduction in retinal artery, ophthalmic artery, or ciliary artery blood flow, leading to a decrease in retinal circulation which, in turn, causes retinal hypoxia.[4] Also, it must be noted that while, classically and most commonly, emboli causing amaurosis fugax are described as coming from an atherosclerotic carotid artery, any emboli arising from vasculature preceding the retinal artery, ophthalmic artery, or ciliary arteries may cause this transient monocular blindness.

  • Atherosclerotic carotid artery: Amaurosis fugax may present as a type of transient ischemic attack (TIA), during which an embolus unilaterally obstructs the lumen of the retinal artery or ophthalmic artery, causing a decrease in blood flow to the ipsilateral retina. The most common source of these thromboemboli is an atherosclerotic carotid artery.[5]
    However, a severely atherosclerotic carotid artery may also cause amaurosis fugax due to its stenosis of blood flow, leading to ischemia when the retina is exposed to bright light.[6] "Unilateral visual loss in bright light may indicate ipsilateral carotid artery occlusive disease and may reflect the inability of borderline circulation to sustain the increased retinal metabolic activity associated with exposure to bright light."[7]
  • Atherosclerotic ophthalmic artery: Will present similarly to an atherosclerotic internal carotid artery.
  • Temporary vasospasm leading to decreased blood flow can be a cause of amaurosis fugax.[8][9] Generally, these episodes are brief, lasting no longer that five minutes,[10] and have been associated with exercise.[4][11] These vasospastic episodes are not restricted to young and healthy individuals. "Observations suggest that a systemic hemodynamic challenge provoke[s] the release of vasospastic substance in the rentinal vasculature of one eye."[10]
  • Giant cell arteritis: Giant cell arteritis can result in granulomatous inflammation within the central retinal artery and posterior ciliary arteries of eye, resulting in partial or complete occlusion, leading to decreased blood flow manifesting as amaurosis fugax. Commonly, amaurosis fugax caused by giant cell arteritis may be associated with jaw claudication and headache. However, it is also not uncommon for these patients to have no other symptoms.[12] One comprehensive review found a two to nineteen percent incidence of amaurosis fugax among these patients.[13]
  • Drug abuse-related intravascular emboli[2]

Ocular origin

Ocular causes include:

Neurologic origin

Neurological causes include:

  • Papilledema: "The underlying mechanism for visual obscurations in all of these patients appear to be transient ischemia of the optic nerve head consequent to increased tissue pressure. Axonal swelling, intraneural masses, and increased influx of interstitial fluid may all contribute to increases in tissue pressure in the optic nerve head. The consequent reduction in perfusion pressure renders the small, low-pressure vessels that supply the optic nerve head vulnerable to compromise. Brief fluctuations in intracranial or systemic blood pressure may then result in transient loss of function in the eyes."[31] Generally, this transient visual loss is also associated with a headache and optic disk swelling.
  • Multiple Sclerosis can cause amaurosis fugax due to a unilateral conduction block, which is a result of demyelination and inflammation of the optic nerve, and "...possibly by defects in synaptic transmission and putative circulating blocking factors."[32]


References

  1. Burde RM. "Amaurosis fugax. An overview." J Clin Neuroophthalmol. 1989 Sep;9(3):185-9. PMID 2529279
  2. 2.0 2.1 2.2 2.3 2.4 2.5 The Amaurosis Fugax Study Group. "Current management of amaurosis fugax." Stroke. 1990;21(2):201-208.
  3. Newman NJ. "Cerebrovascular disease." Walsh & Hoyt's Clinical Neuro-Ophthalmology. (Miller NR, Newman NJ, eds.) Vol 3. 5th ed. Baltimore, Williams & Wilkins; 1998:3420-3426.
  4. 4.0 4.1 "Exercise-Induced Vasospastic Amaurosis Fugax." Arch Ophthalmol. 2002 February;120(2):220-222.
  5. Braat, Andries; Peter H. Hoogland, A.C. DeVries, J.C. Alexander de Mol VanOtterloo. "Amaurosis Fugax and Stenosis of the Ophthalmic Artery." Vascular and Endovascular Surgery. 2001;35(2):141-142.
  6. Kaiboriboon K; Piriyawat P; Selhorst JB. "Light-induced amaurosis fugax." Am J Ophthalmol. 2001 May;131(5):674-6. PMID 11336956.
  7. AU Furlan AJ; Whisnant JP; Kearns TP. "Unilateral visual loss in bright light. An unusual symptom of carotid artery occlusive disease." Arch Neurol. 1979 Nov;36(11):675-6. PMID 508123.
  8. Ellenberger C Jr., Epstein AD. "Ocular complications of atherosclerosis: what do they mean?" Semin Neurol. 1986;6:185-193.
  9. Fisher M. "Transient monocular blindness associated with hemiplegia." Arch Ophthalmol. 1952;47:167-203.
  10. 10.0 10.1 Burger, Stephen; robert Saul, John Selhorst, Stephen Thurston. "Transient monocular blindness caused by vasospasm." The New England Journal of Medicine. 1991;325:870-873.
  11. Imes RK, Hoyt WF. "Exercise-induced transient visual events in young healthy adults." J Clin Neuro Ophthalmol. 1989:9;9:178-180.
  12. AU Hayreh SS; Podhajsky PA; Zimmerman B. "Occult giant cell arteritis: ocular manifestations." Am J Ophthalmol. 1998 Apr;125(4):521-6. PMID 9559738.
  13. Goodman BW Jr. "Temporal arteritis." Am J Med. 1979;67:839-852.
  14. Giorgi, Afeltra, Gabrieli. "Transient visual symptoms in systemic lupus erthematosus and antiphospholipid syndrome." Ocular Immunology and Inflammation. March 2001;9(1):49-57.
  15. Gold D, Feiner L, Henkind P. "Retinal arterial occlusive disease in systemic lupus erythematosus." Arch Ophthalmol. 1977;95:1580-1585.
  16. Newman NM, Hoyt WF, Spencer WH. "Macula-sparing blackouts: clinical and pathologic investigations of intermittent choroidal vascular insufficiency in a case of periarteritis nodosa." Arch Ophthalmol. 1974; 91:367-370.
  17. Schwartz ND, So YT, Hollander H, Allen S, Fye KH. "Eosinophilic vasculitis leading to amaurosis fugax in a patient with acquired immunodeficiency syndrome." Arch Intern Med. 1986;146:2059-2060
  18. 18.0 18.1 18.2 18.3 18.4 Bacigalupi, Michael. "Amaurosis Fugax-A Clinical Review." The Internet Journal of Allied Health Sciences and Practice. April 2006;4(2):1-6.
  19. Berdel, Theiss, Fink, Rastetter. "Peripheral arterial occlusion and amaurosis fugax as the first manifestation of polycythemia vera." Journal Annals of Hematology. 1984;48(3):177-180.
  20. Mundall, Quintero, von Kaulla, Harmon, Austin. "Transient monocular blindness and increased platelet aggregability treated with aspirin." Neurology. 1972;22:280-285.
  21. Smith. "Protein C deficiency: A cause of amaurosis fugax?" Neurol Neurosurg Psychiatry. 1987;50:361-362.
  22. Digre, Durcan, Branch, Jacobson, Varner, Baringer. "Amaurosis fugax associated with antiphospholipid antibodies." Ann Neurol. 1989;25:228-232.
  23. 23.0 23.1 23.2 23.3 23.4 23.5 23.6 23.7 Digre, Kathleen. "Amaurosis Fugax and Not So Fugax—Vascular Disorders of the Eye." Practical Viewing of the Optic Disc. Butterworth Heinemann: November 2002:269-344.
  24. Landi, Calloni, Sabbadini, Mannucci, Candelise. "Recurrent ischemic attacks in two young adults with lupus anticoagulants." Stroke. 1983;14:377-379.
  25. Elias M, Eldor A. "Thromboembolism in patients with the 'lupus'-type circulating anticoagulant." arch Intern Med. 1984;144:510-515.
  26. Hayreh SS, Servais GE, Virdi PS. "Fundus lesions in malignant hypertension, V. hypertensive optic neuropathy." Ophthalmology. 1986;93:74-87.
  27. 27.0 27.1 Sorensen PN. "Amaurosis fugax. A unselected material." Acta Ophthalmol (Copenh). 1983 Aug;61(4):583-8. PMID: 6637419.
  28. Ravits J, Seybold M. "Transient monocular visual loss from narrow-angle glaucoma." Arch Neurol. 1984;41:991-993.
  29. Brown GC, Shields JA. "Amaurosis fugax secondary to presumed cavernous hemangioma of the orbic." Ann Ophthalmol. 1981;13:1205-12O9.
  30. Wilkes SR, Troutmann JC, DeSanto LW, Campbell RJ. "Osteoma. An unusual cause of amaurosis fugax." Mayo Clin Proc. 1979;54:258-260.
  31. AU Hayreh SS; Podhajsky PA; Zimmerman B. "Transient visual obscurations with elevated optic discs." Ann Neurol. 1984 Oct;16(4):489-94. PMID 6497356.
  32. AU Smith KJ; McDonald WI. "The pathophysiology of multiple sclerosis: the mechanisms underlying the production of symptoms and the natural history of the disease." Philos Trans R Soc Lond B Biol Sci. 1999 October 29;354(1390):1649-73. PMID 10603618.
  33. Mattsson, Lundberg. "Characteristics and prevalence of transient visual disturbances indicative of migraine visual aura." Cephalalgia. June 1999;19(5):447.
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