Transient visual loss …

Leanne Stunkel MD

Neuro-Ophthalmology & Neuro-Otology

Updated 09.25.2024
Released 02.08.2001
Expires For CME 09.25.2027

Transient visual loss

Author: Leanne Stunkel MD

See Contributor Disclosures

Editor: Jonathan D Trobe MD

Transient visual loss

In This Article

Quick Link

Introduction

Overview

Transient visual loss, meaning vision loss that resolves spontaneously within 24 hours, can have causes ranging from benign to emergent and potentially catastrophic, making proper evaluation urgent. Any disorder that can cause temporary dysfunction of the afferent visual system, including the eye, retina, optic nerve or tracts, lateral geniculate body, geniculocalcarine tract or striate (calcarine, visual), and peristriate cortices, can cause transient visual loss. As the vision loss is transient, the examination is often unrevealing, making the history particularly essential for diagnosis.

Differentiating monocular from binocular symptoms is the first step toward identifying the etiology. Binocular transient visual loss may be due to posterior circulation ischemia, migraine visual aura, or seizure. Monocular transient visual loss may be due to thromboembolism or vasospasm of the central retinal artery, ocular causes such as acute angle closure glaucoma, and pigmentary dispersion syndrome. Patients with migraine visual aura may also have difficulty accurately determining whether their transient symptoms were monocular or binocular.

For the purposes of this article, transient vision loss refers to relatively brief (hours or shorter) episodes of transient visual loss or transient visual disturbances that resolve spontaneously. Causes of vision loss that are reversible by treating the underlying cause, such as posterior reversible encephalopathy syndrome and hyperglycemic nonketotic homonymous hemianopia, are outside the scope of this review. Conditions that affect the efferent visual system, meaning the oculomotor system, may also cause transient or intermittent visual symptoms, including difficulty focusing, double vision, and oscillopsia, but this article focuses on disorders that cause a transient change to the afferent visual system.

Key points

	• Transient binocular visual loss may be due to posterior circulation ischemia, migraine, or seizure.
	• Transient monocular visual loss may be due to thromboembolism or vasospasm of the central retinal artery; giant cell arteritis; papilledema; ocular causes, such as acute angle closure glaucoma; or other causes, including migraine.
	• The most important job of the clinician is to identify and protect the patient from dangerous causes of transient vision loss (ischemic, arteritic, angle closure glaucoma, papilledema).

Historical note and terminology

The clinical importance of transient monocular visual loss was initially described in detail by Fisher (21; 22; 17), who emphasized that transient visual loss in a single eye may occur due to thromboembolism from severe occlusive disease of the ipsilateral internal carotid artery in the neck. Associated episodes of contralateral hemibody weakness are also suggestive of thromboembolic events due to carotid stenosis. Fisher also described and illustrated the funduscopic findings in a patient who he observed during an attack of transient monocular blindness (19). Pessin and colleagues subsequently showed that a high percentage of patients who had episodic transient monocular visual loss and transient hemispheric dysfunction referable to the ipsilateral cerebral hemisphere had severe stenosis or occlusion of the ipsilateral internal carotid artery (49).

The term “amaurosis fugax,” (“amaurosis” is Greek for darkness, and “fugax” is Latin for “fleeting”) is sometimes used as a synonym for transient monocular vision loss, specifically transient monocular vision loss due to a thromboembolic cause. Some providers may use it as a description of undifferentiated symptoms, and others may assume that it means that a thromboembolic cause has already been confirmed. Given these different usages, this term is imprecise and can mistakenly suggest to other providers that an ischemic etiology has been confirmed; thus, it is best avoided (20; 07; 42).

Clinical manifestations

Presentation and course

	• Localization starts with distinguishing whether a transient visual loss event was monocular or binocular.
	• Taking a detailed history of the event is a key part of diagnosis.
	• Evaluation requires a thorough ophthalmic examination, including ocular surface examination; evaluation of the depth of the anterior chamber; and evaluation for optic disc swelling, retinal emboli, and cotton wool spots, as well as for focal neurologic signs.

Monocular versus binocular

Monocular and binocular visual loss have different localizations. Monocular vision loss localizes to the eye or the anterior visual pathways, whereas binocular vision loss usually localizes to the chiasm or retrochiasmal visual pathways. Some causes of transient vision loss are monocular phenomena that affect both eyes simultaneously. Examples are the transient visual obscurations usually due to papilledema and dry eye syndrome (Table 1).

Providers must be aware that patients may not accurately identify the localization of an episode of transient vision loss. For example, a right hemifield defect affecting both eyes may be described by the patient as vision loss affecting the right eye. During the event, many patients will not have attempted to localize the visual deficit, which is best done by covering one eye and then the other. In cases of ongoing vision loss, examination maneuvers, such as visual acuity testing, color vision testing, the swinging flashlight test, and visual field testing, allow providers to distinguish between monocular and binocular vision loss. However, in cases of transient vision loss, the patient’s history may be the sole source of diagnostic information. Historical clues that can suggest that a transient vision loss event affected both eyes include difficulty reading (which should not be seen in patients with monocular vision loss) and noticing that the visual deficit was limited to a hemifield.

Table 1. Differential Diagnosis of Transient Vision Loss

Transient monocular vision loss	Monocular phenomena that may affect both eyes simultaneously	Transient binocular vision loss
Ischemia (embolic, hypoperfusion, venous congestion, giant cell/temporal arteritis)	Transient visual obscurations from papilledema	Migraine visual aura
Retinal artery vasospasm	Transient intraocular pressure elevations	Posterior circulation transient ischemic attack
Orbital mass (“gaze-evoked amaurosis”)	Dry eye or ocular surface	Occipital lobe seizure
Smartphone amaurosis/transient monocular vision loss on awakening	Uhthoff phenomenon
Transient monocular vision loss on awakening
Vitreomacular traction, hyphema, surgical complications

Further, pinpointing the etiology depends on taking a careful, detailed history to elucidate the character of the vision loss episode (Table 2). However, the patient’s description alone may not allow the physician to determine the cause (07). It is important to have a low threshold and consider ischemic causes in order to protect patients from permanent vision loss and other complications.

Table 2. Aspects Of History Important for Evaluating an Episode of Transient Vision Loss

	• Did the vision loss affect one eye or both eyes?
	• Did the vision loss come on suddenly or gradually?
	• What is the pattern and degree of vision loss (blackout versus blur, respect of vertical, horizontal)?
	• Are there positive visual phenomena?
	• How long did the episode(s) last?
	• How long ago did the episodes start?
	• Are there any provocative factors (positional changes, bright lights, exercise, head, eccentric gaze)?
	• Are there associated symptoms (focal neurologic symptoms, systemic symptoms of giant cell arteritis)?
	• Is there relevant past medical history (vascular risk factors, recent surgeries)?

Transient monocular vision loss

Transient monocular vision loss results from pathology affecting the anterior visual pathways, including the pre-chiasmal optic nerve, retina, and other ocular structures. Even after determining that an episode of transient vision loss is monocular, the differential diagnosis remains broad, including ischemic optic neuropathy, ocular causes, and migraine (Table 1). However, the most common cause of transient monocular vision loss is ischemia (07).

Embolic occlusion of central or branch retinal artery. Ischemic transient monocular vision loss can represent a transient embolic occlusion of the central retinal artery or a branch retinal artery, particularly thromboembolism from carotid disease (67).

This type of transient monocular vision loss is expected to be sudden, painless, and described as a dark “shade,” “curtain,” or complete blackout of vision lasting 1 to 4 minutes. Patients may also describe an altitudinal cut-off or a “line” in their vision. Ischemia is not expected to cause positive visual phenomena, but patients with retinal ischemia occasionally describe shimmering or whiteness, such as “Autumn mist” or “snowing up of a television screen” (19). Examination showing retinal emboli can be supportive of a diagnosis of embolic occlusion, but a normal fundus examination does not rule it out.

Ischemic transient monocular vision loss should be considered a retinal transient ischemic attack equivalent to a cerebral transient ischemic attack. In fact, 20% to 30% of patients who present with transient monocular vision loss have had acute silent strokes on diffusion-weighted imaging (29; 60; 06; 04; 59). A full stroke work-up, including urgent carotid imaging, is appropriate. If the event occurred within the week preceding the examination, emergent work-up is appropriate (06).

Neck pain and ipsilateral Horner syndrome should raise suspicion for cervical carotid artery dissection.

Giant cell arteritis or temporal arteritis. Giant cell arteritis (also known as temporal arteritis) may cause episodes of transient vision loss or transient diplopia, or both. Giant cell arteritis is encountered in elderly patients (16) and is more common in women and Caucasians. It is important to ask patients about systemic symptoms suggestive of giant cell arteritis, such as fever, chills, unintentional weight loss, achy shoulders and hips, headaches, scalp tenderness, and jaw pain evoked by chewing (“jaw claudication”). Jaw claudication improves with rest because the inflamed external carotid artery branches serving the muscles of mastication are not able to respond to the increased perfusion requirements when the muscles are in use. Fundus examination may show additional signs of ischemia, such as cotton wool spots. Fluorescein angiography may show choroidal hypoperfusion. As patients with transient vision loss due to giant cell arteritis are likely to have permanent vision loss within hours of symptom onset, it is essential to have a low threshold for suspecting this diagnosis. Inflammatory markers (ESR, CRP, and platelet count) should be ordered on all patients aged 50 and older who report transient monocular vision loss episodes, even if they do not report additional systemic symptoms.

Ocular hypoperfusion. Severe carotid stenosis may also cause transient monocular vision loss due to hypoperfusion. In this setting, exposure of the retina to intense light, which increases metabolic activity in the retina, may exceed the capacity of the compromised carotid-ophthalmic artery system, leading to transient vision loss due to inadequate ocular perfusion. The vision loss may last up to 5 to 10 minutes and may be precipitated by maneuvers that lower the perfusion pressure, such as standing up, or by maneuvers that increase the metabolic demand on the retina, such as looking at a bright light (“light-induced amaurosis”) (63).

Chronic ocular hypoperfusion may result in ocular ischemic syndrome, damaging the structures of the eye and causing severe eye pain. Examination findings include narrowed retinal arteries; dilated retinal veins; midperipheral retinal hemorrhages; cotton wool spots; microaneurysms; corneal edema; and neovascularization of the iris, optic disc, or retina.

Venous congestion. Venous congestion, such as that due to an impending central retinal vein occlusion, may cause episodic loss of vision for a duration of 10 to 20 minutes. In these cases, ophthalmoscopy discloses tortuosity or dilation of the retinal veins, together with dot-blot retinal hemorrhages.

Central retinal artery vasospasm. Central retinal artery vasospasm is a putative cause of stereotyped episodes of painless transient monocular vision loss that typically last 30 to 60 seconds. Young patients without vascular risk factors are at risk. Some patients report triggers, such as emotional stress, cold, or exercising (62; 35). Ingestion of phencyclidine or cocaine may trigger episodes (64). The vasospasm is typically transient; therefore, a firm diagnosis is not possible as the fundus will not usually be observed during an episode. However, cases have been reported in which the fundus was observed and photographed or videotaped during an episode, showing transient narrowing of the retinal arteries (11; 50; 32; 46). Permanent vision loss is unlikely.

Gaze-evoked amaurosis. An orbital mass may intermittently compress the orbital optic nerve or its feeder arteries. Episodes are typically provoked by eccentric gaze (10; 45; 37; 48). Proptosis elicited on Hertel exophthalmometry is suggestive, and orbital imaging is required in search of a mass.

Angle closure glaucoma. Patients with intermittent closure of the aqueous exit pathway may report episodes of blurry vision and haloes around lights and will typically have severe eye pain and headache during the episodes. Examination during an ictus may show a red eye with a mid-dilated pupil and elevated intraocular pressure. Episodes may be triggered by activities that cause pupillary dilation, such as watching television in a dark room. At other times, examination may look normal other than a narrow anterior chamber angle, which is best seen by examination of the anterior chamber angle with a special instrument called a gonioscope, a procedure that requires the expertise of an ophthalmologist.

Transient smartphone blindness or “smartphone amaurosis.” Transient smartphone blindness describes transient monocular loss of vision occurring immediately after using a smartphone while lying down on one side of the body in a dark or dimly lit environment (01; 33; 56). This benign, physiological phenomenon is caused by unequal light adaptation of the two eyes. The eye ipsilateral to the side on which the subject is lying may be blocked from the illumination of the smartphone screen and become dark adapted. Being exposed to the smartphone’s luminance, the fellow eye becomes light adapted.

After the smartphone has been set aside, there may be transient monocular vision loss in the light-adapted eye that lasts for several minutes. Two authors monocularly viewed a smartphone screen at arm’s length, and the time course of recovery of sensitivity in the dark was quantified both psychophysically and electrophysiologically by means of electroretinography (01). Visual sensitivity was appreciably reduced after smartphone viewing, taking several minutes to recover. Multiple similar cases have been reported (33; 56).

Transient monocular vision loss only on awakening. A study reported 29 patients with transient monocular vision loss present only on awakening that resolved within 15 minutes (09). The patients had undergone extensive negative evaluations. This phenomenon should be suspected if a patient reports transient monocular vision loss occurring only on awakening. The authors proposed a pathogenesis separate from that of unequal light adaptation (smartphone blindness), such as a neurovascular autoregulatory failure resulting in a supply and demand mismatch during low-light conditions.

Additional ocular causes. Hyphema after intraocular surgery can cause temporary visual loss (34; 02), as can sub-Tenon anesthesia given for cataract surgery (18) and leaking blebs following trabeculectomy for glaucoma (24).

A highly stereotyped form of transient monocular vision loss has been reported in several members of two families with familial hemiplegic migraine and an SCN1A mutation (65). Lasting between 3 and 10 seconds, the visual loss could occur spontaneously or be elicited by rubbing the eye, sudden exposure of the eye to bright light, or standing up quickly. Vision loss occurred in both eyes after rubbing merely one eye, with a 1- to 2-second delay before onset in the second eye (39). During an episode, the pupil was dilated and unresponsive to light. The episodes typically occurred multiple times daily for decades without resulting in permanent vision loss (65).

Ocular conditions may produce transient visual loss that occurs in both eyes simultaneously.

Transient visual obscurations. Transient visual obscurations are black-outs or gray-outs of vision lasting 5 to 15 seconds (55). They are usually precipitated by the Valsalva maneuver or by quickly assuming the upright posture. These ultra brief episodes result from high tissue pressure within the optic nerve head, usually due to optic disc edema but also occasionally due to optic nerve head drusen or anomalous optic discs. In these optic disc abnormalities, the transient visual loss may also be monocular.

Uhthoff symptom. Uhthoff symptom is transient vision loss precipitated by a rapid increase in body temperature (44). This phenomenon should be suspected in patients with a history of demyelinating optic neuritis who notice transient recurrent visual blurring after brisk exercise or taking a hot shower.

Pigment dispersion syndrome. Pigment dispersion syndrome is due to an excessive release of pigment (58). The pigment accumulates in the trabecular meshwork and reduces aqueous outflow. Patients may report transient vision loss and haloes around lights. Physical exercise may be a trigger for the episodes. Patients with pigment dispersion syndrome may have iris transillumination defects, pigment on the corneal endothelium or in the anterior chamber, and heavy pigmentation of the trabecular meshwork best seen with gonioscopy.

Dry eye or ocular surface. Patients with dry eye syndrome may report transient visual loss, but further questioning will reveal that this is visual blurring rather than dimness or darkness. They may also notice intermittent monocular diplopia. Symptoms are typically worse later in the day and with activities that decrease blink rate, such as driving, reading, or screen time. Slit lamp examination with fluorescein staining may show superficial punctate epithelial erosions and a decreased tear break-up time.

Transient binocular vision loss

Migraine visual aura. Migraine visual aura is the most common cause of transient binocular vision loss. Patients with transient vision loss due to migraine classically describe stereotyped visual disturbances involving both eyes, nearly always including positive visual phenomena. The positive visual phenomena are usually described as a moving complex of sparkling, shimmering, flickering, rotating, oscillating, or kaleidoscopic lights. The visual disturbance starts in one area of the visual field and spreads or “marches” to involve a larger area. “Fortification spectra” is the term used to describe these phenomena, based on the description of a migraineur who reported that the positive visual phenomena looked like the outline of a fortified town with bastions. As the leading edge of positive visual phenomena spreads, scotomatous vision loss will often be noted in its place. Episodes typically evolve over 15 to 30 minutes and should not last longer than 60 minutes. The visual aura may be followed by a headache with phonophobia and photophobia. However, the presence of headache is not required for the diagnosis (28).

Examination may show a homonymous visual field defect during an episode, but interictal examination should be normal (23).

Red flags that should raise concern for an alternative etiology include sudden onset of the visual disturbance without expansion or migration across the visual field, a less than 20-minute or greater than 60-minute duration of the visual loss, and a persisting homonymous hemianopia.

The perception that the visual episode was monocular should not rule out migraine. Patients often ascribe a binocular homonymous visual phenomenon to the eye with the temporal field cut.

Occipital transient ischemic attack. Patients who have a transient occlusion of the basilar or posterior cerebral arteries may have an episode of homonymous hemianopia. This cause should be suspected when the clinical features of migraine are absent and when there are neurologic symptoms that localize to the vertebrobasilar arterial circulation, including vertigo, dizziness, diplopia, ataxia, and focal weakness. The episodes should not last more than a few minutes. Some patients may report an associated headache.

Seizures. Seizures occurring in the posterior parietal, posterior temporal, and occipital lobes can give rise to temporary visual symptoms and transient homonymous hemianopia. The visual symptoms consist of brief flashes of light. Patients may have other manifestations of seizures, including loss of consciousness or amnesia. Tumors and vascular malformations are the most common causes. In a study of 43 patients with posterior cortical epilepsy, four patients had visual aura described as blurry vision, whereas 14 had “elementary visual hallucinations,” and four had “visual illusions” (72). No one described transient visual blackouts.

Prognosis and complications

Transient intraocular pressure elevations and vitreomacular traction episodes could potentially lead to permanent vision loss, if not treated. Migraine, smartphone blindness, transient monocular vision loss on awakening, central retinal artery vasospasm, and dry eye are benign. Uhthoff symptom demands exclusion of multiple sclerosis.

Patients who have episodes of transient monocular vision loss from an ischemic cause have a serious risk of subsequent permanent vision loss or cerebral stroke. A prospective study showed that transient monocular vision loss episodes preceded the onset of permanent vision loss in a large proportion of 440 eyes with central retinal artery occlusion and branch retinal artery occlusion, 1202 eyes with central retinal vein occlusion and branch retinal vein occlusion, 39 eyes with ocular ischemic syndrome, 946 eyes with non-arteritic anterior ischemic optic neuropathy, and 147 eyes with giant cell arteritis (27).

A prospective study of 341 consecutive patients found that over 4 years following episodes of transient monocular vision loss, 4.4% developed stroke, myocardial infarction, or retinal infarction per year (66).

A prospective study of 198 patients with transient monocular blindness found that the risk of ipsilateral stroke within 3 years ranged from 2% to 24%, depending on the number of additional risk factors (05). A prospective study of 654 patients with an episode of transient or permanent monocular vision loss found that more than 6% had a stroke within the next 5 years and more than 4% had a stroke in the carotid territory ipsilateral to the symptomatic eye, with a higher risk in patients with carotid stenosis (15).

A prospective study capturing 826 patients with transient visual symptoms found that a major embolic source was identified in 20%, and patients with homonymous hemianopia were more likely to have atrial fibrillation than those without (38). A retrospective review of 400 patients with monocular ischemia, including 263 patients with transient monocular vision loss due to ischemia, showed that 14% had ipsilateral carotid stenosis and 9% had atrial fibrillation, likely an underestimate as only 53% of the cohort had undergone prolonged cardiac monitoring (73).

A study of 439 consecutive untreated patients with transient or permanent retinal artery occlusions from 1973 to 2000 showed that more than 65% had ipsilateral carotid artery plaques, 30% had more than 50% ipsilateral carotid artery stenosis, and more than 50% had an abnormal echocardiogram (26). The authors emphasized that patients may have both carotid artery and cardiac disease and that patients should be evaluated for both.

These latter studies were done in the modern era of secondary stroke prevention treatment. The risks are likely to be higher in patients who do not undergo stroke work-up and receive secondary stroke prevention care. Before the era of intensive evaluation and stroke preventive care, patients had even higher rates of major stroke after an initial presentation of transient ischemic attack (06).

Clinical vignette

A week prior to presentation, a 75-year-old man reported that a black shade had descended over his right eye. He had a past medical history of previous coronary artery bypass surgery, hypertension, and claudication of the right leg. After 30 seconds, the shade lifted from the bottom. Two days earlier, he had noted an episode of transient clumsiness and weakness of his left hand that resolved after 3 minutes. During the previous 3 weeks, he had noticed headaches, an unusual symptom for him.

Examination showed a loud, long, high-pitched right carotid artery bruit. A bright cholesterol crystal was seen in his right eye at a bifurcation point distally along a superior retinal artery. The neurologic examination, including visual acuity and visual fields, was otherwise normal.

Duplex sonography showed severe stenosis of the right internal carotid artery, a finding corroborated by CT angiography of the neck. MRI showed no brain infarction. He underwent an uneventful right carotid endarterectomy.

Biological basis

Etiology and pathogenesis

The differential diagnosis of transient vision loss is broad and includes vascular, ophthalmic, and other causes—each with a different pathogenesis. The most relevant etiologies are ischemia and migraine.

Transient ischemia. Transient ischemia of the anterior circulation typically causes transient monocular vision loss, whereas transient ischemia of the posterior circulation typically causes transient binocular vision loss.

Transient monocular vision loss can occur due to ischemia of the anterior circulation. The internal carotid artery’s first major branch is the ophthalmic artery, which gives off the central retinal artery that supplies the retina and the posterior ciliary arteries that supply the optic nerve head. Transient ischemia can occur due to embolism, which originates in an atherosclerotic plaque at the cervical carotid artery bifurcation, or to hypoperfusion, which can occur due to flow-limiting carotid stenosis. Stenosis may involve the common or internal carotid artery (31). Transient monocular vision loss due to stenosis of the ophthalmic artery has also been reported (47). Patients with transient vision loss have a risk of subsequent ischemic stroke, but the risk is not as high as in patients who have had a cerebral transient ischemic attack. A retrospective review of 28 patients with retinal vision loss and 26 patients with transient ischemic attack or middle cerebral artery stroke who had undergone cerebral angiography found that patients who had experienced a retinal ischemic event had a more proximal angular origin of the ophthalmic artery than patients who had experienced a cerebral transient ischemic attack or stroke (54).

Episodes of transient monocular vision loss due to hypoperfusion may be seen in patients with less than 1 mm residual lumen (90% stenosis). The attacks may be brought on by standing up quickly, changes in neck position (eg, during archery or violin playing), or after eating (40). When the internal carotid artery is completely occluded, patients may show periodic dimming of vision when exposed to bright light. Patients with bilateral internal carotid occlusive disease may have binocular dimming of vision on bright light exposure (36).

Carotid artery dissection may also cause transient monocular vision loss if the artery becomes acutely narrowed or occluded. Dissection may be associated with other focal neurologic symptoms due to transient ipsilateral hemispheric ischemia.

Embolism from the heart may also cause transient monocular vision loss (12; 43; 26; 73). Cardiogenic embolism is a less common cause than carotid stenosis (03; 73) but may be underestimated as not all patients undergo long-term cardiac monitoring after a transient monocular vision loss event (73).

Embolism from the aorta is another potential cause, particularly during and after cardiac surgery or angiography.

Transient binocular vision loss can occur due to ischemia of the posterior circulation. Severe stenosis or occlusion or, less often, dolichoectatic dilatation of the intracranial vertebral or basilar arteries can cause an intermittent decrease in blood flow to the occipital lobes. The most common cause of posterior cerebral artery territory infarction is embolism to the posterior cerebral artery from the heart, aorta, or extracranial and intracranial vertebral arteries (13; 71; 38).

Pathophysiology of migraine visual aura. Migraine visual aura is attributed to cortical spreading depression within the occipital cortex. The classic semiology of positive visual phenomena with fortification spectrum is thought to correspond to the anatomy of the occipital cortex (53; 08; 61; 30; 57; 25). Terms such as “retinal migraine,” “ocular migraine,” and “ophthalmic migraine” are sometimes used to describe migraine visual aura. If the visual episode is truly confined to one eye, the diagnosis cannot be migraine, which is strictly a visual cortex phenomenon.

Transient monocular vision loss that lasts for minutes and has no positive visual phenomena is more likely to represent ocular ischemia than migraine (30; 46; 52; 14). Although the term “retinal migraine” is included in the ICHD-3 (28), it is very difficult to meet the diagnostic criteria, and some commentators have argued that the term is a misnomer—an outdated term for central retinal artery vasospasm based on the historical theory of migraine as a vasospastic process (68; 14).

Management

Treatment is dictated by the cause of the transient visual loss. Management of angle closure glaucoma and orbital pathology should be delegated to ophthalmologists. The following causes are treated by neurologists.

Ischemia. A stroke work-up should be done to assess risk factors in patients who have a suspected ischemic cause of transient monocular or binocular vision loss (41). Secondary stroke prevention treatments should be initiated. Patients with atrial fibrillation will be treated with anticoagulation. Patients with transient monocular vision loss who have internal carotid artery stenosis may be candidates for carotid endarterectomy or angioplasty with stenting.

Arteritis. If there is suspicion of giant cell arteritis/temporal arteritis, the patient should immediately be treated with high-dose corticosteroids to prevent permanent loss of vision predominantly due to ischemic optic neuropathy. High-dose corticosteroid therapy is initiated immediately in high-risk cases. Once the diagnosis is confirmed by a positive temporal artery biopsy, the patient must be treated continuously with oral corticosteroids or steroid-sparing agents, typically over the course of at least 1 year. A rheumatologist can help manage the corticosteroid course or use of steroid-sparing agents.

Seizures. Seizures must be treated with anticonvulsants.

Migraine visual aura. Reassurance that the episodes are benign and will not lead to permanent vision loss is very helpful for patients with migraine visual aura. Some patients are not bothered by infrequent episodes once reassured of their benign nature. If the episodes are bothersome, headache hygiene (hydration, sleep, avoidance of triggers) is appropriate. Pharmacologic migraine prophylaxis can also be helpful for reducing the frequency of episodes. Abortive medications are not helpful for the treatment of migraine visual aura as the onset will not be quick enough to prevent the aura. However, a migraine abortive taken at the time the visual aura is first noticed may be helpful in preventing headache in patients who typically have a severe headache following the aura.

Central retinal artery vasospasm. Reassurance that the episodes are benign and will not lead to permanent vision loss is helpful. If the patient is bothered by frequent episodes, calcium channel blockers may decrease the frequency (70; 69; 51).

Papilledema. After a work-up to evaluate for the underlying cause of papilledema, medications such as acetazolamide, topiramate, and furosemide may be used to lower intracranial pressure. Surgical management, such as ventriculoperitoneal shunt, optic nerve sheath fenestration, or transverse dural venous sinus stenting, may be indicated in severe, vision-threatening cases.

References

01: Alim-Marvasti A, Bi W, Mahroo OA, Barbur JL, Plant GT. Transient smartphone “blindness.” N Eng J Med 2016;374(25):2502-4. PMID 27332920
02: Ambresin A, Borruat FX, Mermoud A. Recurrent transient visual loss after deep sclerotomy. Arch Ophthalmol 2001;119:1213-5. PMID 11483096
03: Anderson DC, Kappelle LJ, Eliasziw, M, Babikian VL, Pearce LA, Barnett HJ. Occurrence of hemispheric and retinal ischemia in atrial fibrillation compared with carotid stenosis. Stroke 2002;33:1963-8. PMID 12154246
04: Ayrignac X, Zagroun C, Coget A, et al. Acute retinal arterial ischaemia: silent brain infarcts prevalence and short-term recurrence. Eur J Neurol 2020;27(12):2517-22. PMID 32810911
05: Benavente O, Eliasziw M, Streifler JY, et al. Prognosis after transient monocular blindness associated with carotid-artery stenosis. N Engl J Med 2001;345(15):1084-90. PMID 11596587
06: Biousse V, Nahab F, Newman NJ. Management of acute retinal ischemia: follow the guidelines! Ophthalmology 2018;125(10):1597-607. PMID 29716787
07: Biousse V, Trobe JD. Transient monocular visual loss. Am J Opthalmol 2005;140(4):717-21. PMID 16140247
08: Bolay H, Moskowitz MA. The emerging importance of cortical spreading depression in migraine headache. Rev Neurol (Paris) 2005;161(6-7):655-7. PMID 16141950
09: Bouffard MA, Cornblath WT, Rizzo JF, et al. Transient monocular vision loss on awakening: a benign amaurotic phenomenon. J Neuroophthalmol 2017;37(2):122-5. PMID 27749399
10: Brown GC, Shields JA. Amaurosis fugax secondary to presumed cavernous hemangioma of the orbit. Ann Ophthalmol 1981;13(10):1205-9. PMID 7316347
11: Burger SK, Saul RF, Selhorst JB, Thurston SE. Transient monocular blindness caused by vasospasm. N Eng J Med 1991;325(12):870-3. PMID 1875972
12: Caplan LR. Brain embolism. In: Caplan LR, Hurst JW, Chimowitz MI. Clinical neurocardiology. New York: Marcel Dekker, 1999:35-185.
13: Caplan LR. Posterior circulation disease. Clinical findings, diagnosis, and management. Boston: Blackwell Science, 1996.
14: Chong YJ, Mollan SP, Logeswaran A, Sinclair AB, Wakerley BR. Current perspective on retinal migraine. Vision (Basel) 2021;5(3):38. PMID 34449754
15: De Schryver ELLM, Algra A, Donders RCJM, van Gijn J, Kappelle LJ. Type of stroke after transient monocular blindness or retinal infarction of presumed arterial origin. J Neurol Neurosurg Psychiatry 2006;77(6):734-8. PMID 16500944
16: Douglas VP, Rachapudi SS, Davila-Siliezar P, Laylani NAR, Lee AG. Transient monocular visual loss (amaurosis fugax): how does age impact diagnosis? Ophthalmol Ther 2024;13(6):1417-25. PMID 38587773
17: Estol CJ. Miller Fisher and the history of carotid artery disease. Stroke 1996;27(3):559-66. PMID 8610329
18: Feibel RM, Guyton DL. Transient central retinal artery occlusion after posterior sub-Tenon's anesthesia. J Cataract Refract Surg 2003;29(9):1821-4. PMID 14522307
19: Fisher CM. Observations of the fundus oculi in transient monocular blindness. Neurology 1959;9:333-47. PMID 13657292
20: Fisher CM. 'Transient monocular blindness' versus 'amaurosis fugax.' Neurology 1989;39(12):1622-4. PMID 2685658
21: Fisher M. Occlusion of the internal carotid artery. AMA Arch Neurol Psychiatry 1951;65(3):346-77. PMID 14810286
22: Fisher M. Transient monocular blindness associated with hemiplegia. AMA Arch Ophthalmol 1952;47(2):167-203. PMID 14894017
23: Goodwin D. Transient complete homonymous hemianopia associated with migraine. Optometry 2011;82(5):298-305. PMID 21524601
24: Grigorian AP, Spaeth G. An explanation of transient visual loss associated with leaking filtering bleb. Am J Opthalmol 2004;138(5):869-70. PMID 15531329
25: Hansen JM, Baca SM, Vanvalkenburgh P, Charles A. Distinctive anatomical and physiological features of migraine aura revealed by 18 years of recording. Brain 2013;136(Pt 12):3589-95. PMID 24264937
26: Hayreh SS, Podhajsky PA, Zimmerman MB. Retinal artery occlusion: associated systemic and ophthalmic abnormalities. Ophthalmology 2009;116(10):1928-36. PMID 19577305
27: Hayreh SS, Zimmerman MB. Amaurosis fugax in ocular vascular occlusive disorders: prevalence and pathogeneses. Retina 2014;34(1):115-22. PMID 23632956
28: Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2018;38(1):1-211. PMID 29368949
29: Helenius J, Arsava EM, Goldstein JN, et al. Concurrent acute brain infarcts in patients with monocular visual loss. Ann Neurol 2012;72(2):286-93. PMID 22926859
30: Hill DL, Daroff RB, Ducros A, Newman NJ, Biousse V. Most cases labeled as "retinal migraine" are not migraine. J Neuroophthalmol 2007;27(1):3-8. PMID 17414865
31: Hsu HY, Yang FY, Chao AC, et al. Distribution of carotid arterial lesions in Chinese patients with transient monocular blindness. Stroke 2006;37:531-3. PMID 16373651
32: Inoue T, Shimizu H, Okabe H, Tominga T. Amaurosis fugax caused by retinal artery vasospasm. Case illustration. J Neurosurg 2007;106(5):934. PMID 17542546
33: Irshad F, Adhiyaman V. Transient smartphone blindness. Can J Ophthalmol 2017;52(3):e107-8. PMID 28576218
34: Jacobson D, Gloor P. Recurrent transient monocular visual impairment caused by hyphema following intraocular surgery. Neurology 1988;38:163. PMID 3336451
35: Jehn A, Dettwiler F, Fleischhauer B, Sturznegger M, Mojon DS. Exercise-induced vasospastic amaurosis fugax. Arch Ophthalmol 2002;120:220-2. PMID 11831932
36: Kaiboriboon K, Piriyawat P, Selhorst JB. Light-induced amaurosis fugax. Am J Ophthalmol 2001;131:674-6. PMID 11336956
37: Knapp ME, Flaherty PM, Sergott RC, Savino PJ, Mazzoli RA, Flanagan JC. Gaze-induced amaurosis from central retinal artery compression. Ophthalmology 1992;99:238-40. PMID 1553214
38: Lavallee PC, Cabrejo L, Labreuche J, et al. Spectrum of transient visual symptoms in a transient ischemic attack cohort. Stroke 2013;44(12):3312-7. PMID 24178913
39: Le Fort D, Safran AB, Picard F, Bouchardy I, Morris MA. Elicited repetitive daily blindness: a new familial disorder related to migraine and epilepsy. Neurology 2004;63(2):348-50. PMID 15277634
40: Levin LA, Mootha VV. Postprandial transient visual loss. A symptom of critical carotid stenosis. Ophthalmology 1997;104:397-401. PMID 9082262
41: Mbonde AA, O'Carroll CB, Dulamea OA, Anghel D, Chong BW, Dumitrascu OM. Current guidelines on management of amaurosis fugax and transient ischemic attacks. Asia Pac J Ophthalmol (Phila) 2022;11(2):168-76. PMID 35213421
42: Miller NR, Newman NJ, Biousse V, Kerrison JB. Walsh and Hoyt’s clinical neuro-ophthalmology. 6th edition. Philadelphia: Lippincott Williams & Wilkins, 2005.
43: Mouradian M, Wijman CA, Tomasian D, Davidoff R, Koleini B, Babikian V. Echocardiographic findings of patients with retinal ischemia or embolism. J Neuroimaging 2002;12(3):219-23. PMID 12116739
44: Opara JA, Brola W, Wylegala AA, Wylegala E. Uhthoff’s phenomenon 125 years later - what do we know today? J Med Life 2016;9(1):101-5. PMID 27974923
45: Orcutt JC, Tucker WM, Mills RP, Smith CH. Gaze-evoked amaurosis. Ophthalmology 1987;94(3):213-8. PMID 3587895
46: Ota I, Kuroshima K, Nagaoka T. Fundus video of retinal migraine. JAMA Ophthalmol 2013;131(11):1481-2. PMID 24008349
47: Park MS, Kim JT, Lee KR, et al. Recurrent transient monocular blindness with ophthalmic artery stenosis. Eur Neurol 2008;59(3-4):202-4. PMID 18230884
48: Patel MM, Lefebvre DR, Lee NG, Brachtel E, Rizzo J, Freitag SK. Gaze-evoked amaurosis from orbital breast carcinoma metastasis. Ophthal Plast Reconstr Surg 2013. PMID 23446302
49: Pessin MS, Duncan GW, Mohr JP, Poskanzer DC. Clinical and angiographic features of carotid transient ischemic attacks. N Engl J Med 1977;296:358-62. PMID 834199
50: Petzold A, Islam N, Plant GT. Video reconstruction of vasospastic transient monocular blindness. N Eng J Med 2003;348(16):1609-10. PMID 12700390
51: Pitkanen H, Saarela V. Vasospastic transient monocular visual loss: effect of treatment with different doses of nifedipine. J Neuroophthalmol 2014;34(4):386-8. PMID 24905274
52: Pula JH, Kwan K, Yuen CA, Kattah JC. Update on the evaluation of transient vision loss. Clin Ophthalmol 2016;10:297-303. PMID 26929593
53: Richards W. The fortification illusions of migraines. Sci Am 1971;224(5):88-96. PMID 5552581
54: Rossin EJ, Gilbert AL, Koen N, Leslie-Mazwi TM, Cunnane ME, Rizzo JF 3rd. Site of origin of the ophthalmic artery influences the risk for retinal versus cerebral embolic events. J Neuroophthalmol 2021;41(1):24-8. PMID 31985565
55: Sadun AA, Currie JN, Lessell S. Transient visual obscurations with elevated optic discs Ann Neurol 1984;16(4):489-94. PMID 6497356
56: Sathiamoorthi S, Wingerchuk DM. Transient smartphone blindness: relevance to misdiagnosis in neurologic practice. Neurology 2017;88(8):809-10. PMID 28100724
57: Schott GD. Exploring the visual hallucinations of migraine aura: the tacit contribution of illustration. Brain 2007;130(Pt 6):1690-703. PMID 17264093
58: Scuderi G, Contestabile MT, Scuderi L, Librando A, Fenicia V, Rahimi S. Pigment dispersion syndrome and pigmentary glaucoma: a review and update. Int Ophthalmol 2019;39(7):1651-62. PMID 29721842
59: Smith CE, Kukolja J. Prevalence and risk factors of ischemic monocular vision loss and concurrent brain ischemia. Eur Stroke J 2023;8(4):982-8. PMID 37593943
60: Tanaka K, Uehara T, Kimura K, et al. Features of patients with transient monocular blindness: a multicenter retrospective study in Japan. J Stroke Cerebrovasc Dis 2014;23(3):e151-5. PMID 24144597
61: Teive HA, Kowacs PA, Maranhao Filho P, Piovesan EJ, Werneck LC. Leao’s cortical spreading depression: from experimental "artifact" to physiological principle. Neurology 2005;65(9):1455-9. PMID 16275835
62: Teman AJ, Winterkorn JM, Weiner D. Transient monocular blindness associated with sexual intercourse. N Engl J Med 1995;333(6):393. PMID 7609772
63: Ting RJE, Hui M, Thoo C, Coroneo MT, Francis IC. Light-induced amaurosis: a rare manifestation of internal carotid artery stenosis. Cureus 2019;11(10):e5817. PMID 31737459
64: Ubogu E. Amaurosis fugax associated with phencyclidine inhalation. Eur Neurol 2001;46(2):98-9. PMID 11528160
65: Vahedi K, Depienne C, Le Fort D, et al. Elicited repetitive daily blindness: a new phenotype associated with hemiplegic migraine and SCN1A mutations. Neurology 2009;72(13):1178-83. PMID 19332696
66: Volkers EJ, Donders RC, Koudstaal PJ, van GJ, Algra A, Jaap KL. Transient monocular blindness and the risk of vascular complications according to subtype: a prospective cohort study. J Neurol 2016;263(9):1771-7. PMID 27314958
67: Weiss V, Doležalová I, Mňuk T, Labounková I, Herzig R, Nestrašil I. Teaching video neuroImage: amaurosis fugax due to recurrent central retinal artery occlusion by microemboli. Neurology 2022;99(7):313-4. PMID 35750495
68: Winterkorn JM. "Retinal migraine" is an oxymoron. J Neuroophthalmol 2007;27(1):1-2. PMID 17414864
69: Winterkorn JM, Kupersmith M, Wirtschafter JD, Forman S. Brief report: treatment of vasospastic amaurosis fugax with calcium channel blockers. N Engl J Med 1993;329:396-8. PMID 8326973
70: Winterkorn JM, Teman AJ. Recurrent attacks of amaurosis fugax treated with calcium channel blockers. Ann Neurol 1991;30:423-5. PMID 1952830
71: Yamamoto Y, Georgiadis AL, Chang HM, Caplan LR. Posterior cerebral artery territory infarcts in the New England Medical Center (NEMC) Posterior Circulation Registry. Arch Neurol 1999;106:824-32. PMID 10404984
72: Yu T, Wang Y, Zhang G, Cai L, Du W, Li Y. Posterior cortex epilepsy: diagnostic considerations and surgical outcome. Seizure 2009;18(4):288-92. PMID 19136282
73: Zarkali A, Cheng SF, Dados A, Simister R, Chandratheva A. Atrial fibrillation: an underestimated cause of ischemic monocular visual loss? J Stroke Cerebrovasc Dis 2019;28(6):1495-9. PMID 30935808

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Leanne Stunkel MD

Dr. Stunkel of Washington University in St. Louis has no relevant financial relationships to disclose.
See Profile

Editor

Jonathan D Trobe MD

Dr. Trobe of the University of Michigan has no relevant financial relationships to disclose.
See Profile

Former Authors

Louis R Caplan MD
Omar Solyman MD
James Goodwin MD
Heather E Moss MD PhD

Patient Profile

Age range of presentation: 0 month to 65+ years
Sex preponderance: None
Heredity: None
Population groups selectively affected: No population group selectively affected
Occupation groups selectively affected: No occupation group selectively affected

ICD & OMIM codes

ICD-10: Transient visual loss, unspecified eye: H53.129

Unqualified visual loss, both eyes: H54.3

Unqualified visual loss, one eye: H54.6

Unspecified visual loss: H54.7

Suppression of binocular vision: H53.3
ICD-11: Transient visual loss: 9D51

Amaurosis fugax: 8B10.0

This is an article preview.
Start a Free Account
to access the full version.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Questions or Comment?

MedLink®, LLC

3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122

Toll Free (U.S. + Canada): 800-452-2400

US Number: +1-619-640-4660

Support: service@medlink.com

Editor: editor@medlink.com

ISSN: 2831-9125

Transient visual loss

Associated Disorders

angle closure glaucoma
anomalous optic discs
branch retinal artery occlusion
carotid stenosis
central retinal artery occlusion
- central retinal artery vasospasm
- demyelinating disease
- dry eye
- giant cell arteritis
- idiopathic intracranial hypertension/pseudotumor cerebri
- intracranial hypertension
- migraine
- narrow angles
- optic nerve head drusen
- optic neuritis
- orbital mass
- papilledema
- pigmentary dispersion syndrome
- posterior circulation stroke
- seizures
- temporal arteritis
- transient ischemic attack
- transient monocular blindness
- transient ocular ischemia
- Uhthoff phenomena
- visual aura
- vitreomacular traction

Differential Diagnosis

transient monocular vision loss
monocular phenomena that may affect both eyes simultaneously
transient binocular vision loss

Also Relevant

Amaurosis fugax
Cortical blindness
Ischemic optic neuropathy
Retinal migraine
Temporal arteritis

Transient visual loss …

Transient visual loss

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Monocular versus binocular

Table 1. Differential Diagnosis of Transient Vision Loss

Table 2. Aspects Of History Important for Evaluating an Episode of Transient Vision Loss

Transient monocular vision loss

Transient binocular vision loss

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Diagnostic workup

Management

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

NF2-related schwannomatosis

Neurogenetics and genetic and genomic testing

Acute traumatic spinal cord injury

Tumors of the skull base

Common maculopathies

Toxic and nutritional deficiency optic neuropathies

Third nerve palsy

Nystagmus

Transient visual loss

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Monocular versus binocular

Table 1. Differential Diagnosis of Transient Vision Loss

Table 2. Aspects Of History Important for Evaluating an Episode of Transient Vision Loss

Transient monocular vision loss

Transient binocular vision loss

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Diagnostic workup

Management

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

NF2-related schwannomatosis

Neurogenetics and genetic and genomic testing

Acute traumatic spinal cord injury

Tumors of the skull base

Common maculopathies

Toxic and nutritional deficiency optic neuropathies

Third nerve palsy

Nystagmus

This is an article preview.
Start a Free Account
to access the full version.