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Amaurosis Fugax

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Sohan Singh Hayreh – One of the best experts on this subject based on the ideXlab platform.

Bridget M Zimmerman – One of the best experts on this subject based on the ideXlab platform.

  • Amaurosis Fugax in ocular vascular occlusive disorders prevalence and pathogeneses
    Retina-the Journal of Retinal and Vitreous Diseases, 2014
    Co-Authors: Sohan Singh Hayreh, Bridget M Zimmerman
    Abstract:

    Purpose To investigate systematically the prevalence of Amaurosis Fugax (AF) in various ocular vascular occlusive disorders individually and to discuss the pathogeneses of each. Methods The study comprised patients with central retinal artery occlusion (271 eyes), branch retinal artery occlusion (169 eyes), ocular ischemic syndrome (39 eyes), central retinal vein occlusion (864 eyes), hemi-central retinal vein occlusion (67 eyes), branch retinal vein occlusion (285 eyes), nonarteritic anterior ischemic optic neuropathy (946 eyes), and giant cell arteritis with visual loss (147 eyes). At first visit, all patients had a detailed ophthalmic and medical history and comprehensive ophthalmic evaluation and systemic evaluation. Results Prevalence of AF was 12.18% in central retinal artery occlusion, 14.20% in branch retinal artery occlusion, 15.38% in ocular ischemic syndrome, 4.86% in central retinal vein occlusion, 37.84% in central retinal vein occlusion with cilioretinal artery occlusion, 13.43% in hemi-central retinal vein occlusion, 0.35% in branch retinal vein occlusion, and 2.54% in nonarteritic anterior ischemic optic neuropathy. In giant cell arteritis, 32.4% of patients with ocular involvement had a history of AF or 26.5% of the involved eyes. Amaurosis Fugax in central retinal artery occlusion, branch retinal artery occlusion, and nonarteritic anterior ischemic optic neuropathy is mostly because of transient embolism. The pathogenesis of AF in each ocular vascular occlusive disorder is discussed. Conclusion Prevalence and pathogenesis of AF in various ocular vascular occlusive disorders varies widely. Amaurosis Fugax may be the presenting symptom in these disorders and that always requires urgent evaluation.

Ping Wang – One of the best experts on this subject based on the ideXlab platform.

  • Amaurosis Fugax caused by heritable thrombophilia hypofibrinolysis in cases without carotid atherosclerosis thromboprophylaxis prevents subsequent transient monocular partial blindness
    Clinical and Applied Thrombosis-Hemostasis, 2007
    Co-Authors: Charles J Glueck, Karl C. Golnik, Ping Wang
    Abstract:

    Nineteen patients (age 60 ± 14) with Amaurosis Fugax associated with heritable thrombophilia-hypofibrinolysis without ipsilateral atherosclerotic carotid plaque or other causes of Amaurosis Fugax were studied. Our hypothesis was that case-specific thromboprophylaxis would prevent subsequent Amaurosis Fugax episodes. Prospective treatment data were available for 13 cases. Thrombophilic disorders included high Factors VIII and XI, G20210A prothrombin heterozygosity, low proteins C and S, MTHFR mutations, and the PL A1/A2 mutation. Hypofibrinolytic disorders included plasminogen activator inhibitor-1 4G4G, and high lipoprotein (a). Treatments included Coumadin; Lovenox, folic acidvitamin B6-vitamin B12, discontinuation of estrogens-selective estrogen receptor modulators, Glucophage, and aspirin, as appropriate. Usually within 1 month on therapy, patients became asymptomatic and have remained asymptomatic for ≥ 1 year on therapy, without adverse treatment side effects. When Amaurosis Fugax occurs without car…

  • Amaurosis Fugax caused by heritable thrombophilia-hypofibrinolysis in cases without carotid atherosclerosis: thromboprophylaxis prevents subsequent transient monocular partial blindness.
    Clinical and applied thrombosis hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis Hemostasis, 2007
    Co-Authors: Charles J Glueck, Karl C. Golnik, Ping Wang
    Abstract:

    Nineteen patients (age 60 +/- 14) with Amaurosis Fugax associated with heritable thrombophilia-hypofibrinolysis without ipsilateral atherosclerotic carotid plaque or other causes of Amaurosis Fugax were studied. Our hypothesis was that case-specific thromboprophylaxis would prevent subsequent Amaurosis Fugax episodes. Prospective treatment data were available for 13 cases. Thrombophilic disorders included high Factors VIII and XI, G20210A prothrombin heterozygosity, low proteins C and S, MTHFR mutations, and the PL A1/A2 mutation. Hypofibrinolytic disorders included plasminogen activator inhibitor-1 4G4G, and high lipoprotein (a). Treatments included Coumadin; Lovenox, folic acidvitamin B6-vitamin B12, discontinuation of estrogens-selective estrogen receptor modulators, Glucophage, and aspirin, as appropriate. Usually within 1 month on therapy, patients became asymptomatic and have remained asymptomatic for > or = 1 year on therapy, without adverse treatment side effects. When Amaurosis Fugax occurs without carotid arteartery atherosclerosis or other known causes, thrombophilia or hypofibrinolysis, or both are nearly universal, safely treatable, reversible pathoetiologies.

  • Amaurosis Fugax: Associations with Heritable Thrombophilia
    Clinical and applied thrombosis hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis Hemostasis, 2005
    Co-Authors: C. J. Glueck, Naila Goldenberg, Howard Bell, Karl C. Golnik, Ping Wang
    Abstract:

    The aim of this study was to prospectively assess associations between Amaurosis Fugax, inherited thrombophilia, and acquired thrombophilia. Thrombophilia and hypofibrinolysis were studied in 11 cases (eight women, three men; all white) with Amaurosis Fugax, 57 +/- 17 years old, selected by the absence of abnormal brain magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), magnetic resonance venography (MRV), ipsilateral internal carotid arteartery plaque, atrial fibrillation, or cardiac thrombus. Cases were compared to 78 healthy adult white controls (53 +/- 18 years old) for serologic measures, and by polymerase chain reaction to 248 healthy white controls (78 adults, 170 children) for gene mutations. All 11 cases had one or more familial thrombophilic coagulation disorder including one heterozygous for the G1691A factor V Leiden mutation, two with low free protein S, four with high factor VIII, three with resistance to activated protein C, three homozygous for the C677T methylenetetrahydrofolate reductase (MTHFR) mutation, two compound C677T-A1298C MTHFR heterozygotes, and three with hypofibrinolytic 4G4G homozygosity for the PAI-1 gene. The case with factor VIII of 160% had two other thrombophilias (compound MTHFR C677T-A1298C heterozygosity, resistance to activated protein C), and hypofibrinolytic high Lp(a). Thrombophilic C677T MTHFR homozygosity or compound C677T-A1298C heterozygosity was present in five of 10 (50%) cases vs. 30 of 248 (12%) controls, Fisher’s p (p(f)) = .005. Thrombophilic factor VIII was high in four of 10 (40%) cases vs. 0 of 38 controls, p(f) = .001. Thrombophilic hyperestrogenemia in five of the eight women (four exogenous estrogen, one pregnant) may have interacted with inherited thrombophilia-hypofibrinolysis, promoting thrombus formation. In cases selected by the absence of abnormal brain magnetic resonance imaging, significant ipsilateral internal carotid arteartery plaque, atrial fibrillation, or cardiac thrombus, we speculate that Amaurosis Fugax can be caused by reversible (by anticoagulation) retinal artery thrombi associated with heritable thrombophilia and/or hypofibrinolysis, often augmented by estrogen-driven acquired thrombophilia.

Peter J. Koudstaal – One of the best experts on this subject based on the ideXlab platform.

  • The source of embolism in Amaurosis Fugax and retinal artery occlusion.
    International ophthalmology, 1994
    Co-Authors: Roland L. M. J. Smit, G. Seerp Baarsma, Peter J. Koudstaal
    Abstract:

    To assess the diagnostic value of an extensive cardiac screening and of carotid arteartery duplex scanning in patients suspected of suffering from retinal embolism, we examined 41 consecutive patients (mean age 59.6 years, range 36–74) who presented either with Amaurosis Fugax or with a retinal artery occlusion. In spite of extensive investigations, we found no cause in 27 patients (66%). In 11 patients (27%), symptoms were likely to be due to a stenosis or an occlusion of the ipsilateral carotid arteartery. In only 1 patient (2%), the heart was likely to be a source of embolism. We conclude that in patients in this age group suffering from either Amaurosis Fugax or a retinal artery occlusion, a carotid arteartery duplex scanning should be performed first as this investigation is more likely to provide useful information than an extensive cardiac screening (ECG, Holler 24-hour monitoring and precordial echocardiography).

Charles J Glueck – One of the best experts on this subject based on the ideXlab platform.

  • Amaurosis Fugax caused by heritable thrombophilia hypofibrinolysis in cases without carotid atherosclerosis thromboprophylaxis prevents subsequent transient monocular partial blindness
    Clinical and Applied Thrombosis-Hemostasis, 2007
    Co-Authors: Charles J Glueck, Karl C. Golnik, Ping Wang
    Abstract:

    Nineteen patients (age 60 ± 14) with Amaurosis Fugax associated with heritable thrombophilia-hypofibrinolysis without ipsilateral atherosclerotic carotid plaque or other causes of Amaurosis Fugax were studied. Our hypothesis was that case-specific thromboprophylaxis would prevent subsequent Amaurosis Fugax episodes. Prospective treatment data were available for 13 cases. Thrombophilic disorders included high Factors VIII and XI, G20210A prothrombin heterozygosity, low proteins C and S, MTHFR mutations, and the PL A1/A2 mutation. Hypofibrinolytic disorders included plasminogen activator inhibitor-1 4G4G, and high lipoprotein (a). Treatments included Coumadin; Lovenox, folic acid-vitamin B6-vitamin B12, discontinuation of estrogens-selective estrogen receptor modulators, Glucophage, and aspirin, as appropriate. Usually within 1 month on therapy, patients became asymptomatic and have remained asymptomatic for ≥ 1 year on therapy, without adverse treatment side effects. When Amaurosis Fugax occurs without car…

  • Amaurosis Fugax caused by heritable thrombophilia-hypofibrinolysis in cases without carotid atherosclerosis: thromboprophylaxis prevents subsequent transient monocular partial blindness.
    Clinical and applied thrombosis hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis Hemostasis, 2007
    Co-Authors: Charles J Glueck, Karl C. Golnik, Ping Wang
    Abstract:

    Nineteen patients (age 60 +/- 14) with Amaurosis Fugax associated with heritable thrombophilia-hypofibrinolysis without ipsilateral atherosclerotic carotid plaque or other causes of Amaurosis Fugax were studied. Our hypothesis was that case-specific thromboprophylaxis would prevent subsequent Amaurosis Fugax episodes. Prospective treatment data were available for 13 cases. Thrombophilic disorders included high Factors VIII and XI, G20210A prothrombin heterozygosity, low proteins C and S, MTHFR mutations, and the PL A1/A2 mutation. Hypofibrinolytic disorders included plasminogen activator inhibitor-1 4G4G, and high lipoprotein (a). Treatments included Coumadin; Lovenox, folic acid-vitamin B6-vitamin B12, discontinuation of estrogens-selective estrogen receptor modulators, Glucophage, and aspirin, as appropriate. Usually within 1 month on therapy, patients became asymptomatic and have remained asymptomatic for > or = 1 year on therapy, without adverse treatment side effects. When Amaurosis Fugax occurs without carotid artery atherosclerosis or other known causes, thrombophilia or hypofibrinolysis, or both are nearly universal, safely treatable, reversible pathoetiologies.