Tra n s i e n t M o n o c u l a r

Visual Loss
Rehan Ahmed, MD, Rod Foroozan, MD*

KEYWORDS
 Transient monocular visual loss  Amaurosis fugax
 Transient monocular blindness

Transient monocular visual loss (TMVL) is the preferred term for the abrupt loss of
visual function in one eye that lasts less than 24 hours.1,2 The terms ‘‘amaurosis fugax’’
(translating from Greek to mean ‘‘fleeting blindness’’) and ‘‘transient monocular blind-
ness’’ are sometimes used by clinicians interchangeably with ‘‘transient monocular
visual loss.’’ However, ‘‘amaurosis fugax’’ does not specify whether the loss is in
one or both eyes, and the term also implies visual loss secondary to ischemic
causes.1,3 As shown in Box 1, there are a number of nonischemic causes of TMVL.
The term ‘‘transient monocular blindness’’ implies a complete loss of vision, but
most episodes of TMVL cause only a partial loss of vision.2 As TMVL may be nonische-
mic in etiology, incomplete, and strictly refers only to monocular visual loss, it has
been suggested that this term be used in preference to others.4
We limit our discussion to conditions that typically cause monocular visual loss. It is
crucial to remember, however, that a patient’s perception of monocular versus binoc-
ular visual loss can be misleading. Patients with binocular hemifield (homonymous)
visual loss often localize visual loss only to the eye that lost the temporal visual field.4
It is important to ask if visual loss was noted in the fellow eye when the affected eye
was covered during the episode. In addition, patients with binocular visual loss also
tend to have a more pronounced reading impairment, whereas monocular visual
loss does not usually impair reading unless the unaffected eye has a prior visual
impairment.2
Establishing whether the visual loss is monocular or binocular helps to localize the
lesion: monocular visual loss results from a lesion anterior to the chiasm (the eye or
optic nerve), whereas binocular visual loss may be from lesions to both eyes or optic
nerves, or, much more likely, from lesions to the chiasm or retrochiasmal pathways.
The most important step in the clinical evaluation of any patient presenting with tran-
sient visual loss (TVL) is to obtain a thorough history. The age of the patient, the dura-
tion of visual loss, the pattern of visual loss and recovery, and any associated

Cullen Eye Institute, Baylor College of Medicine, 7200B Cambridge Street, Houston, TX 77030,
USA
* Corresponding author.
E-mail address: foroozan@bcm.edu

Neurol Clin 28 (2010) 619–629

doi:10.1016/j.ncl.2010.03.004 neurologic.theclinics.com
0733-8619/10/$ – see front matter ª 2010 Elsevier Inc. All rights reserved.
620 Ahmed & Foroozan

Box 1
Causes of transient monocular visual loss

Typically Associated with Abnormal Eye Examination

Ocular Pathology (nonvascular)
Blepharospasm
Tear film abnormalities
Keratoconus
Intermittent angle-closure glaucoma
Vitreous debris
Orbitopathy
Orbital masses and foreign bodies
Optic Nerve
Papilledema
Optic nerve drusen/Congenital optic disc anomalies
Compressive lesions of the intraorbital optic nerve
Demyelinating disease
Retina
Age-related macular degeneration
Macular disease and photostress
Retinal detachment
Vascular Disease
Ocular hypoperfusion (ocular ischemic syndrome)
Internal/Common carotid artery stenosis
Embolic phenomenon
Carotid
Cardiac
Great vessels
Carotid artery dissection
Vasculitis
Arterial vasospasm (during acute episode)
Hypercoagulable state
Typically Associated with Normal Eye Examination
Vascular Disease
Internal/common carotid artery stenosis
Hypotension
Neurologic
Migraine (including retinal migraine)
Uhthoff’s phenomenon (demyelination)
Nonphysiologic visual loss
 Transient Monocular Visual Loss 621

symptoms or additional signs are all used to formulate a differential diagnosis and
initiate an appropriate management plan.
Despite the importance of obtaining a complete history, the approach to TMVL that
we have found most useful is determining whether the patient has abnormal eye
examination findings that can explain the visual loss.

TMVL WITH AN ABNORMAL EYE EXAMINATION

Patients with abnormalities in the external structures (eg, proptosis), ocular surface,
anterior chamber of the eye, vitreous, optic disc, or retina can all present with TMVL.
Anterior Segment Pathology
Blurred vision caused by an irregularity of the corneal tear film may cause moments of
visual loss. Patients may complain of pain and ocular irritation. Visual acuity is typically
improved with pinhole. Examination using a slit-lamp may reveal an abnormal-appear-
ing tear film and cornea, with punctate keratopathy indicative of dry eyes (sicca
syndrome). The visual symptoms may improve with blinking or the application of
a tear supplement. Measuring the production of tears with a Schirmer test may confirm
poor tear production.5 Corneal epithelial basement membrane dystrophy can also
cause episodes of visual loss, and it is typically associated with pain.6
Opacities in the anterior chamber can also cause TMVL. For example, uveitis-glau-
coma-hyphema (UGH) syndrome is an uncommon complication of cataract extraction
with intraocular lens implantation and presents with a triad of anterior uveitis, glau-
coma, and hyphema.7,8 Typically, the patient has a sudden decrease in vision within
minutes, with a resolution of the symptoms over hours to days.7 This may be associ-
ated with pain, and a microhyphema may be seen if the patient is examined during an
acute episode. There is not a complete loss of light perception. The patient may also
complain of erythropsia (perception of red in the vision) and an ache in the affected eye
owing to associated anterior uveitis or raised intraocular pressure (IOP). Episodes of
TMVL may correlate with inflammation and recurrent bleeding. Gonioscopy may be
required to make the diagnosis. Treatment is required for UGH syndrome if the
repeated episodes of visual disturbance are disabling or glaucoma develops. Defini-
tive treatment involves surgical intraocular lens rotation, exchange, or removal.9
TMVL accompanied by haloes, pain, and nausea should prompt suspicion for
angle-closure glaucoma, although it can rarely occur with painless TMVL.10 The raised
IOP leads to corneal clouding owing to edema and may reduce the perfusion pressure
of the eye, thereby impairing blood flow to the retina and optic disc.11 Intermittent
angle closure tends to recur over days to weeks and is usually less severe than acute
angle-closure glaucoma. The episodes resolve on their own and between episodes
the IOP can be normal, although the presence of glaukomflecken, anterior opacities
on the lens surface, may indicate prior episodes of angle closure.
Retinopathy
Transient visual loss or prolonged afterimages following bright light may be suggestive
of a macular disorder, such as retinal detachment or age-related macular degenera-
tion.12 It is thought that in age-related macular degeneration, the retinal pigment
epithelium and photoreceptor interaction is anatomically deranged causing abnormal
processing of light as it bleaches the rhodopsin in the photoreceptors.13 Abnormalities
in the retina consistent with macular degeneration, such as drusen, would be detected
on funduscopy. Performing the photostress test (10 seconds of exposure to a bright
622 Ahmed & Foroozan

light) shows that the return to normal central visual acuity is abnormally prolonged (>45
seconds).14
Optic Disc Edema
Optic disc edema is an important cause of TMVL. Patients experience brief (<10
seconds) episodes of ‘‘grayouts’’ or ‘‘blackouts’’ of vision. These episodes, termed
transient visual obscurations, are often precipitated by postural changes, although
they may occur spontaneously.4 Dimming of vision lasts for a few seconds, may
involve one eye at a time, and resolves completely. Episodes may recur multiple times
in the day, are thought to be attributable to transient ischemia of the optic nerve head,
and can also occur with optic disc edema that is not related to increased intracranial
pressure.15 Patients may have other symptoms associated with elevated intracranial
pressure, such as headache. These obscurations of vision are not a warning sign of
impending visual failure.16 Neuroimaging should be urgently sought to exclude a struc-
tural etiology such as a mass lesion, venous sinus thrombosis, or obstructive hydro-
cephalus. If imaging is normal, patients should undergo lumbar puncture for
measurement of opening pressure and cerebrospinal fluid analysis.16 Treatment is
aimed at the underlying cause of elevated intracranial pressure.
Other optic disc anomalies such as optic nerve head drusen can also cause tran-
sient visual loss.17 TMVL or even permanent monocular visual loss owing to optic
disc drusen can occur without signs of vascular complications.18 Nevertheless, it is
important that compression by a mass lesion not be overlooked in patients with severe
visual loss, especially in patients with loss of central vision.19 The underlying mecha-
nism of TMVL from optic disc drusen is thought to be similar to causes of optic disc
edema.15 If not directly visible on funduscopy, imaging with ultrasonography or
computed tomography (CT) may be required to demonstrate their presence. Fundu-
scopy may also reveal tortuous vessels, and dilated veins that are often present
with optic disc drusen. Optic disc drusen can be a harbinger for vascular complica-
tions including central retinal artery occlusion and anterior ischemic optic
neuropathy.19
Orbitopathy
Orbital masses or foreign bodies can cause episodic TMVL in certain fields of gaze,
especially downgaze.20 Clues to the diagnosis may include unilateral proptosis on
external examination and restriction in ocular motility. Gaze-evoked episodes most
often are the result of intraconal pathology, most commonly optic nerve sheath menin-
gioma and cavernous hemangioma.21 The common etiology in these patients appears
to be compromise of the retinal or optic nerve circulation, either by means of compres-
sion of the central retinal artery or disruption of the optic nerve microvasculature.22
Interestingly, patients may be unaware of positional visual loss and the ability to
improve this condition with appropriate surgical therapy suggests that all patients
with an orbital disease process should be screened for gaze-evoked visual loss.20
Testing for gaze-evoked visual loss is performed by having the patient look in all direc-
tions of gaze, having the patient hold each eccentric position of gaze for at least 5
seconds, and noting any changes in visual function or pupil reactivity.
Blepharospasm
Patients with blepharospasm who are unable to keep their eyes open may experience
moments of visual loss. This is typically easily distinguished from other causes of
visual loss. In advanced cases, the eyelids cannot be manually opened during an
episode.23
 Transient Monocular Visual Loss 623

Vascular
Emboli
As a result of retinal arteriolar emboli, the patient typically describes a curtain of dark-
ness that descends over one eye, resulting in vision loss lasting 20 to 30 minutes.24,25
With resolution, the curtain may either ascend or slowly disappear. Emboli that cause
TMVL travel and lodge within blood vessels that supply the optic nerve, retina, or
choroid. Funduscopy is warranted because the emboli often appear distinctive and
can provide clues about the possible site of origin, although the absence of emboli
on examination does not exclude them as a cause. The 3 most common types of
emboli are cholesterol, platelet-fibrin, and calcium.26 Their appearance and common
sites of origin are reviewed in Table 1. Other less common causes include emboli from
cardiac tumors (myxoma), fat, sepsis, talc, air, silicone, and depot drugs.16
An embolic cause of TMVL requires vascular and cardiac evaluation. Atheroma
formation is most common at the bifurcation of the internal and external carotid
arteries, but can originate from the heart (eg, in patients with valvular heart disease
or atrial fibrillation) and atheromatous plaque in the aortic arch.27 Emboli may also
arise from the common carotid28 or from carotid dissection.29 Rarely, emboli may orig-
inate from an atrial myxoma,30 or travel from the systemic venous system to the arterial
system via a cardiac septal defect or pulmonary shunt.31
Carotid Doppler ultrasound, which allows an estimation of the degree of stenosis, is
often used initially to screen for internal carotid artery (ICA) stenosis. The atheroma can
remain stationary, become fibrotic, regress, ulcerate, narrow and occlude the lumen,
or release emboli. CT and magnetic resonance (MR) angiography are other useful
screening tests for ICA stenosis, but catheter angiography remains the gold-standard
technique.32 Echocardiography can identify structural cardiac abnormalities associ-
ated with thrombus formation and systemic or paradoxic embolism. In patients with
vascular risk factors, initial imaging with carotid Doppler ultrasound and an echocar-
diogram is typically performed. Regardless of what imaging studies are ultimately
pursued, the presence of retinal emboli allows an opportunity to screen for modifiable
risk factors such as hypertension, diabetes mellitus, and dyslipidemia.

Table 1
Clinical aspects of common retinal emboli

Type Appearance Source

Cholesterol Yellow-orange or copper color Common or internal carotid artery
Refractile Rarely from aorta or innominate
Rectangular artery
Usually located at major vessel
bifurcation
Platelet-fibrin Dull gray-white color From wall of atherosclerotic vessel
Long, smooth shape Heart valves
Concave meniscus at each end
Lodge along course of vessel
Calcium Chalky white From heart or great vessels
Large Rheumatic heart disease
Round or ovoid Calcific aortic stenosis
Lodge at first or second vessel
bifurcation, often overlying disc

Data from Miller N. Embolic causes of transient monocular visual loss. Ophthalmol Clin North Am
1996;9:359–80.
624 Ahmed & Foroozan

The management of TMVL from retinal embolism is directed at the underlying

cause. In patients with a cardiac source, treatment consists of anticoagulation with
warfarin and addressing the underlying cardiac disease with careful attention to
arteriosclerotic risk factors.16 In those with ICA stenosis, antiplatelet therapy with
aspirin should be initiated and vascular risk factors appropriately addressed.33 The
management of high-grade ICA (70%–99%) stenosis with isolated TMVL remains
controversial. The North American Symptomatic Carotid Endarterectomy Trial
suggests that 3 or more of the following risk factors should be present to gain a benefit
from carotid endarterectomy: age older than 75, male gender, history of hemispheric
transient ischemic attack or stroke, history of intermittent claudication, ipsilateral ICA
stenosis of 80% to 94%, and absence of intracranial collateral vessels on cerebral
angiography.33 Carotid stenting may produce equivalent long-term outcomes and
may be a safer option, but additional data are required.16

Retinal vein occlusion

TMVL has also been reported as a symptom of an impending central retinal vein occlu-
sion (CRVO).34 The episodes can last 2 to 4 hours, longer than is typical for transient
arterial retinal ischemia. Patients may complain of cloudiness of vision rather than
frank visual loss typically associated with arterial ischemia.35 On examination, there
may be dilated retinal veins; within 2 weeks, the classic ophthalmoscopic appearance
of CRVO may be present, which includes scattered intraretinal hemorrhages.35
Causes of retinal vein disorders include hypercoaguable states, retinal artery occlu-
sion, and arteriosclerosis. In young patients, further laboratory investigation should
include anticardiolipin antibody, antiphosphatidyl choline and serine, antinuclear anti-
body, serum protein electrophoresis, partial thromboplastin time, and protein S and
protein C to exclude hyperviscosity and hypercoagulability.36 In addition, compressive
orbitopathies and carotid-cavernous fistulas can cause orbital venous hypertension.4

Giant cell arteritis

Among patients with visual manifestations of giant cell arteritis (GCA), a history of tran-
sient visual loss is reported 30% to 54% of the time.37–39 In some patients, transient
visual loss may be the only complaint,40 and precedes the development of acute and
permanent visual loss in more than half (50%–64%) of untreated patients by an
average of almost 9 days.38,41 TMVL results from insufficient perfusion of the optic
nerve, retina, or choroid. GCA typically causes a relatively short duration of visual
loss (<2 minutes), multiple recurrences in the same eye over a short period of time,
photopsias or other phenomena during the visual loss, and visual loss with postural
change such as standing up or bending down.40 In addition, a history of headache,
jaw claudication, scalp tenderness, polymyalgia rheumatica, or systemic symptoms
such as fever, weight loss, or anorexia may suggest the diagnosis. Funduscopic
examination may reveal cotton-wool spots, intraretinal hemorrhages, or optic disc
edema.37 Laboratory markers urgently assessed in suspicious cases include erythro-
cyte sedimentation rate, C-reactive protein, and platelet count.29 The diagnosis is
confirmed with a temporal artery biopsy, characterized by the chief pathologic finding
of a panarteritis consisting mostly of lymphocytes and macrophages.42 Although the
temporal artery biopsy is considered the gold-standard test for the diagnosis, it is
important to remember that a negative biopsy has been said to occur in up to 10%
to 15% of all patients diagnosed clinically as having GCA.43 TMVL may be a warning
symptom for impending anterior ischemic optic neuropathy,44 and early treatment
with corticosteroids may prevent permanent visual loss in patients with TMVL. The
optimal dosage and route of corticosteroids remain unclear.
 Transient Monocular Visual Loss 625

Ocular ischemic syndrome

TMVL can occur from hypoperfusion as a result of stenosis or occlusion of the ipsi-
lateral internal or common carotid arteries. Patients typically describe a dark or black
shade that spreads across the visual field that, unlike TMVL from embolic sources, is
more gradual in onset and can last for seconds to minutes.16 It is often precipitated
by exposure to bright light,45,46 but can occur after meals,47 postural changes,48 or
sexual activity.49 There also can be signs of the ocular ischemic syndrome, which
encompasses a spectrum of findings that result from chronic ocular hypoperfusion.
Ocular ischemic syndrome is relatively uncommon, and the diagnosis may be difficult
to make because of its variable presentations. A history of TMVL is present in
approximately 10% to 15% of patients with ocular ischemic syndrome.50 The pres-
ence of the syndrome implies underlying severe carotid occlusive disease.51 Anterior
segment examination may show dilated conjunctival and episcleral vessels, and
signs of an anterior chamber inflammatory reaction.52 The episcleral injection may
be a sign of collateral blood flow from the external carotid artery in the presence
of an internal carotid artery occlusion.53 Chronic ischemia may also cause iris neo-
vascularization that can lead to increased IOP and neovascular glaucoma.54 Some
patients, however, have an IOP in the normal range, or even ocular hypotony owing
to ischemia of the ciliary body and reduced aqueous humor production.55 On fundu-
scopy, the retinal arteries are generally narrowed, and the retinal veins are often
irregularly dilated with venous beading.55 There may be dot and blot hemorrhages
in the mid-peripheral retina, microaneurysms, cotton-wool spots, and neovasculari-
zation.54 The episodes of visual loss decrease and the risk of further ischemic
damage to the eye is reduced when the stenosis is relieved or the occlusion is
bypassed; underlying vascular risk factors should be addressed to prevent future
vascular events.54

TMVL WITH A NORMAL EYE EXAMINATION

Hypoperfusion
Reduced cardiac output or systemic hypotension may produce TMVL.4 Although
systemic hypotension is typically associated with binocular visual loss, in addition
to lightheadedness and confusion, the combination of a hypotensive episode and
asymmetric anterior circulation stenosis may cause TMVL alone, particularly orthos-
tatically induced TMVL.2
Migraine
Episodes of TMVL designated ‘‘retinal migraine’’ or ‘‘ocular migraine’’ occur in patients
with a history or family history of migraine.56 The International Headache Society diag-
nostic criteria for retinal migraine require at least 2 attacks of fully reversible monoc-
ular-positive visual phenomena such as flashing lights or scintillating scotomas and/
or negative symptoms associated with a headache that fulfills diagnostic criteria for
migraine without aura.57 This is in contrast to a typical migraine with aura, which
involves the cerebral cortex and is associated with binocular visual phenomena.
Retinal migraine affects about 1 of every 200 patients who have migraine, and patients
tend to be younger, with most younger than 40 years.58 Clinically, retinal migraine has
a highly variable presentation. Some patients describe visual loss consisting of black,
gray, white, or shaded areas of varying size that may progress inward from the periph-
eral visual field.56 Most events are transient, lasting from 5 to 20 minutes, and may
occur several times a day. When headaches occur in association with the visual
changes, they may occur either during or after the visual disturbances.58 It should
626 Ahmed & Foroozan

be noted, however, that the existence of retinal migraine is a contested issue, and it
may remain as a diagnosis of exclusion.59,60
Retinal Artery Vasospasm
Similar attacks of TMVL, but without an associated headache, can arise as a result of
retinal artery vasospasm, and do not represent the previously mentioned retinal
migraine.61 In the case of retinal vasospasm, the eye examination may be abnormal
during an attack of visual loss. A relative afferent pupillary defect may be noted or
retinal vasospasm may be observed during funduscopy.62 Patients report attacks of
visual loss that are frequent, recurring many times a day, and often have temporary,
complete monocular visual loss rather than loss restricted to the inferior or superior
altitudinal visual field.63 Attacks of transient monocular visual loss attributable to vaso-
spasm may be treated with calcium channel blockers.63 In either case of retinal
migraine or retinal vasospasm, other causes of TMVL should be excluded as part of
the diagnostic evaluation.16

SUMMARY

TMVL is an important clinical complaint and has a number of causes, of which the
most common is retinal ischemia. A practical approach is to perform a careful exam-
ination to determine whether there are any eye abnormalities that can explain the
visual loss. Despite the transient nature of the symptom, there may be clues to the
diagnosis on the examination even after the visual loss has recovered.

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