Prior to 1990,<unk>  could, "clinically, be divided into four identifiable symptom complexes, each with its underlying pathoetiology: embolic, hypoperfusion, angiospasm, and unknown". In 1990, the causes of<unk>  were better refined by the<unk>  Study Group, which has defined five distinct classes of transient monocular blindness based on their supposed cause: embolic, hemodynamic, ocular, neurologic, and idiopathic (or "no cause identified"). Concerning the pathology underlying these causes (except idiopathic), "some of the more frequent causes include atheromatous disease of the internal carotid or ophthalmic artery, vasospasm, optic neuropathies, giant cell arteritis, angle-closure glaucoma, increased intracranial pressure, orbital compressive disease, a steal phenomenon, and blood hyperviscosity or hypercoagulability." 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. While, most commonly, emboli causing<unk>  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:<unk>  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 athero-emboli is an atherosclerotic carotid artery. However, a severely atherosclerotic carotid artery may also cause<unk>  due to its stenosis of blood flow, leading to ischemia when the retina is exposed to bright light. "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." * Atherosclerotic ophthalmic artery: Will present similarly to an atherosclerotic internal carotid artery. * Cardiac emboli: Thrombotic emboli arising from the heart may also cause luminal obstruction of the retinal, ophthalmic, and/or ciliary arteries, causing decreased blood flow to the ipsilateral retina; examples being those arising due to (1) atrial fibrillation, (2) valvular abnormalities including post-rheumatic valvular disease, mitral valve prolapse, and a bicuspid aortic valve, and (3) atrial myxomas. * Temporary vasospasm leading to decreased blood flow can be a cause of<unk> . Generally, these episodes are brief, lasting no longer than five minutes, and have been associated with exercise. These vasospastic episodes are not restricted to young and healthy individuals. "Observations suggest that a systemic hemodynamic challenge provokes the release of vasospastic substance in the retinal vasculature of one eye." * 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<unk> . Commonly,<unk>  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. One comprehensive review found a two to nineteen percent incidence of<unk>  among these patients. * Systemic lupus erythematosus * Periarteritis nodosa * Eosinophilic vasculitis * Hyperviscosity syndrome * Polycythemia * Hypercoagulability * Protein C deficiency * Antiphospholipid antibodies * Anticardiolipin antibodies * Lupus anticoagulant * Thrombocytosis * Subclavian steal syndrome * Malignant hypertension can cause ischemia of the optic nerve head leading to transient monocular visual loss. * Drug abuse-related intravascular emboli * Iatrogenic:<unk>  can present as a complication following carotid endarterectomy, carotid angiography, cardiac catheterization, and cardiac bypass. Ocular origin Ocular causes include: * Iritis * Keratitis * Blepharitis * Optic disc drusen * Posterior vitreous detachment * Closed-angle glaucoma * Transient elevation of intraocular pressure * Intraocular hemorrhage * Coloboma * Myopia * Orbital hemangioma * Orbital osteoma * Keratoconjunctivitis sicca testing Neurologic origin Neurological causes include: * Optic neuritis * Compressive optic neuropathies * 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." Generally, this transient visual loss is also associated with a headache and optic disk swelling. * Multiple sclerosis can cause<unk>  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." * Migraine * Idiopathic Intracranial Hypertension * Intracranial tumor * Psychogenic
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Nablus mask-like facial syndrome