Lecture Companion Material

Welcome to the learning and teaching companion website for Transient Visual Loss by Randy H. Kardon, MD, PhD, University of Iowa, Iowa City, Iowa USA.
Below you’ll find a Primer of Transient Visual Loss and multiple Case Studies that are meant to completed before viewing the lectures by Dr. Kardon.

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Primer of Work Up for Transient Visual Loss:

Important to understand the mechanism!

Definition of transient visual loss: for the purpose of this primer and our discussions, transient visual loss can mean one or more episodes of visual loss of any duration, monocular or binocular.

Mechanisms of Transient Visual Loss - Monocular

  1. Decrease in ocular perfusion pressure
    1. Fixed arterial stenosis with drop in blood pressure
    2. Vascular occlusive disease (giant cell arteritis), greater on one side compared to the other side, with drop in blood pressure
    3. Severe transient hypotension (orthostatic or heart dysrhythmia) in the setting of greater vascular resistance on one side, compared to the other side or in an eye with asymmetric papilledema.
    4. Central retinal vein occlusion with cilioretinal artery (which has a lower perfusion pressure than central retinal artery) caused by a drop in perfusion pressure in the setting of high retinal venous pressure. This causes a drop in blood flow to the cilioretinal artery with resulting transient visual field loss in the area supplied by the cilioretinal artery.
    5. Vasospasm of central retinal artery
    6. Venous stasis retinopathy with cilioretinal artery hypoperfusion and drops in BP
    7. Acute rise in intraocular pressure (angle closure, pigmentary dispersion, immediately following intravitreal injection)
  2. Embolic (cholesterol, platelet emboli, calcific), rarely fat emboli or talc particles
  3. Compressive – gaze evoked TVL from optic nerve meningioma or orbital mass, or orbital air
  4. Uthoff’s phenomenon (e.g. after demyelination)
  5. Optic nerve drusen (mechanism not completely understood, but presumed to be vascular).
  6. Hyphema – uveitis-glaucoma-hyphema (UGH) syndrome (can be long duration – hours to a day)
  7. Vitreous hemorrhage (longer duration; usually weeks)
  8. Optical: dry eye, but this is more of blurring or monocular diplopia symptom and not a true absence of loss of visions
  9. Photostress – after looking at a bright object and then looking away, but usually bilateral, unless only one eye is exposed to bright light

Mechanisms of Transient Visual Loss – Binocular; orthostatic or heart dysrhythmia (negative, darkening of vision) vs. occipital activation from migraine or seizure (positive visual phenomena)

  1. Decrease in ocular perfusion pressure – transient hypotension; usually the peripheral field starts to close in towards the center and then the central visual field may go out. Peripheral retinal arterioles have a lower ocular perfusion pressure, so that area of the retinal is the first to start to black out as ocular perfusion pressure drops.
  2. Decrease in visual cortex occipital pole perfusion pressure – transient hypotension; in most people, the occipital pole corresponding to the central visual field, lies in a watershed zone, so that a drop in perfusion pressure (e.g. low blood pressure) will cause the central visual field to black out first, before the peripheral visual field.
  3. Migraine – usually white out of vision or positive visual phenomena (geometric shapes are common or “heat-wave” phenomenon), often homonymous but the patient thinks it is one eye (e.g. a patient complaining of right eye transient vision loss may really be right homonymous phenomena)
  4. Occipital seizure – usually positive visual phenomena and often colors, but may be negative visual loss (dark) if post-ictal
  5. Macular degeneration or edema in the macula (e.g. central serous retinopathy or diabetic macular edema) - looking at a bright light and then seeing an afterimage – may be due to photoreceptor dysfunction. Dark spot in the center of vision may also be noticed on awakening in patients with macular disease due to increase in metabolic demand of photoreceptors in darkness; the membrane dark current is maintained by Na+/K+ pump which is ATP energy dependent.

History - It follows from the understanding of the mechanism of transient visual loss

Bilateral vs Unilateral

Bilateral – retina vs. occipital cortex; is center of visual field going out first (occipital drop in perfusion pressure) or is peripheral visual field going out first (retinal drop in perfusion pressure)? The retina macula arterioles have the highest perfusion pressure, so drops in blood pressure affect the peripheral retina first. The occipital pole in visual cortex often lies in a watershed zone of perfusion between the distal branches of the posterior cerebral artery and the middle cerebral artery, so that drops in blood pressure often affect the occipital pole first (corresponding the central visual field).

Unilateral - which part of the visual field went out – peripheral, first, then central (implies drop in ocular perfusion pressure), altitudinal (implies embolic), area of vision spared (central due to cilioretinal artery) or central field only – may be involvement of cilioretinal artery

Duration (seconds, minutes, hours, day)

Transient visual obscurations (seconds) – often occurs in the context of a swollen optic nerve due to severe papilledema with superimposed postural drops in blood pressure

Amaurosis (minutes) – usually due to emboli

Hours – Uveitis Glaucoma Hyphema Syndrome (UGH syndrome) from haptic of intraocular lens rubbing against back of iris after cataract surgery, occipital lobe epilepsy (post-ictal temporary blindness after the seizure)

Characteristics of the episode

Darkening of vision (negative phenomena)? – usually ischemic

White out of vision (positive phenomena)? – usually migraine

“Positive” complex visual phenomena – sparkles, colors, geometric shapes (migraine like aura)

What was the person doing at the time?

Valsalva from coughing or laughing or straining – – may be paradoxical embolism through patent foramen ovale and Valsalva may accentuate right to left shunt of venous thrombi (e.g. from extremity). Sometimes an intense coughing episode may dislodge an intimal plaque or cause a dysrhythmia.

change in posture – orthostatic drop in blood pressure

sitting at rest – suspect either embolism or drop in blood pressure due to dysrhythmia

rubbing their eye – may cause transient spike of intraocular pressure with resulting decrease in ocular perfusion pressure and decrease in blood flow

transient visual loss precipitated by eye movement in extreme gaze – suspicious for compressive optic neuropathy in the orbit (e.g. optic nerve sheath meningioma)

transient visual loss with increase in body temperature (environmental, exercise, hot shower) – suspect demyelination with Uthoff’s phenomena from delayed nerve conduction caused by increases in core body temperature

looking at a bright light and then seeing an afterimage – may be due to photoreceptor dysfunction. Dark spot in the center of vision may also be noticed on awakening in patients with macular disease due to increase in metabolic demand of photoreceptors in darkness; the membrane dark current is maintained by Na+/K+ pump which is ATP energy dependent.

post-prandial, after eating – (“steal phenomena” in the setting of flow significant stenosis)

occurring with exposure to bright daylight – – increase in metabolic demand that cannot be met by increases in blood flow due to flow significant arterial stenosis

palpitations, irregular heartbeat – – transient drops in blood pressure with reduced ocular perfusion pressure, decrease in blood flow; if there is a superimposed arterial stenosis, then the transient visual loss may be unilateral

darkness – angle closure from mydriasis and pupil block with raised IOP

What is the pattern of the vision loss?

Peripheral field goes out first – consider retinal hypoperfusion episode due to transient hypotension (peripheral retinal arterioles have a lower perfusion pressure compared to macular arterioles)

Central field goes out first –– consider occipital pole of visual cortex (lying within a watershed zone) responding to transient hypoperfusion in the setting of a drop in blood pressure.

Regional visual field change such as altitudinal loss – common with embolic cause

Were there any other symptoms at the time?

Light headedness – think about transient hypotension

Unilateral weakness or numbness (TIA) – consider embolic cause

Global amnesia or cognitive dysfunction or motor activation - consider seizure activity


Anterior segment – signs of causes of acute rises in IOP (pigmentary dispersion, narrow angles) or signs of hyphema or microhyphema, iris transillumination defects, IOL haptic rubbing on posterior iris surface.

Posterior segment – signs of emboli (platelet, calcific, cholesterol), venous stasis retinopathy with cilioretinal artery. Digital pressure on globe during exam to determine if small increases in IOP can collapse the central retinal artery or cilioretinal artery due to low ocular perfusion pressure (e.g. carotid stenosis); sometimes this will reproduce the transient darkening of vision. Disc edema associated with raised intracranial pressure may give rise to transient visual obscurations with drops in blood pressure brought on by postural changes or Valsalva maneuver.

Neck bruits

Pulse - any irregularities due to dysrhythmia?

Laboratory testing

Vascular imaging – Duplex ultrasound of carotid and vertebral arteries (is there a significant stenosis or the presence of intimal plaques? But this only samples the cervical portion of the carotid – need MRA or CTA or angiogram to evaluate more distal vascular pathology.

Cardiac echography – is there an embolic source (valves) or patent foramen ovale (bubble study)?

Holter monitor - to discover transient dysrhythmia +/- 24 hour ambulatory blood pressure monitoring to uncover transient episodes of hypotension.

Fluorescein angiography –is there a delay in choroidal filling (giant cell arteritis)? Is there a prolonged arteriole-venular filling time indicative of low ocular perfusion pressure?

CT and/or MRI - to evaluate for any compressive lesion adjacent to the optic nerve. After trauma with orbital fractures, assess if there is intra-orbital air.

Blood testing for coagulopathies – (antiphospholipid antibodies, clotting disorders)

Causes that you will need to think about/differentiate:

Unilateral or Bilateral Transient Visual Obscurations (TVO’s); black outs lasting seconds:
  1. Optic nerve edema due to papilledema (may be asymmetric and only having them on one eye)
  2. Optic nerve drusen
  3. Bleaching of the retina from having just looked at a bright light

Unilateral Amaurosis
  1. Transient decrease in blood supply to the retina or optic nerve due to an embolism (could be cholesterol, calcific, or platelet) – think about the source (heart PFO, heart valve, aorta, carotid, distal to carotid
  2. Transient decrease in blood supply to the retina due to hypoperfusion from a drop in blood pressure (may have a superimposed narrowing of the carotid artery or posterior ciliary artery on one side, e.g. giant cell arteritis) or increase in venous pressure from a transiently hypo-perfused cilioretinal artery in the context of a Central Retinal Vein Occlusion with a sudden drop in blood pressure, or episode of heart dysrhythmia with transiently reduced cardiac output and lowering of blood pressure
  3. Metabolic demand increases in the setting of ocular ischemic syndrome (amaurosis with exposure to bright light or post-prandial, after a meal)
  4. Transient decrease in blood flow to the eye due to increase in intraocular pressure from angle closure glaucoma, intravitreal gas with chronically increased IOP and superimposed transient drops in blood pressure
  5. Transient decrease in blood flow to the retina or optic nerve due to orbital blood or air or mucocele.
  6. Transient decrease in blood flow to the retina due to vasospasm of central retinal artery (especially in the setting of migraine)
  7. Gaze evoked amaurosis due to orbital tumor such as optic nerve sheath meningioma

Bilateral Amaurosis – drops in blood pressure
  1. Retinal – should be peripheral field blacking out first and closing into central field.
  2. Occipital visual cortex (need to understand concept of watershed zone in the occipital pole depending on that person’s dual blood supply from the posterior cerebral artery and middle cerebral artery – usually center of field goes out first

Long Duration Transient Unilateral Visual Loss – hours to days
  1. Blood in anterior chamber (due to IOL haptic rubbing on iris) – usually described as a white out of constant haziness of vision like looking through a fog
  2. Blood in vitreous – can still be from IOL haptic if the posterior lens capsule is not intact or can be from a source of vitreous hemorrhage (retinal tear, neovascularization)
  3. Occipital seizure with post-seizure loss of neuronal firing due to membrane potential hyperpolarization after the seizure

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Quick Guide

Diagnosis Unilateral vs Bilateral Duration Activity Pattern of VL Other Symptoms Medications
Acute Elevation in Intraocular Pressure Unilateral minutes to hours being in a dark environment may precipitate angle closure; physical activity may cause pigmentary dispersion and sudden increase in IOP, ocuarl trauma with hyphema and spike in IOP, eye rubbing may be diffuse blurring if corneal edema results from high IOP; decrease in ocular perfusion pressure will cause peripheral loss of vision first, then central ocular pain adrenergic agents or anticholinergic agents given either systemically or from eye exposure
After-image after viewing bright light Unilateral/Bilateral seconds to minutes viewing bright light, worse after mydriasis usually central after-image none none
Carotid Artery Stenosis with Episode of Hypotension Unilateral minutes (amaurosis fugax) orthostatic or decrease in cardiac output from heart dysrhythmia peripheral field loss first, then possibly followed by central field loss may experience pre-syncopal symptoms or TIA anti-hypertensive agents with over-treatment
Corneal Surface Disease / Dry Eye Unilateral seconds to minutes often tasks requiring concentration which reduces spontaneous blinking, wind or air movement diffuse blurring or monocular diplopia, which may become less after each blink irritation of eye anticholinergic drugs reducing tear production
Giant Cell Arteritis Unilateral/Bilateral seconds to minutes orthostatic changes in posture may be partial or complete loss headaches, jaw claudication, transient diplopia, scalp tenderness,s constitutional symptoms (fatigue, weight loss) none
Hypotension Unilateral/Bilateral seconds to minutes orthostatic changes in posture peripheral field loss first, then possibly followed by central field loss, if retinal ischemia is present, but if occipital pole is affected by low blood pressure, then central field may go out first may experience pre-syncopal symptoms or TIA anti-hypertensive agents with over-treatment
Migraine Bilateral minutes to almost an hour no particular activity, sometimes activities that precipitate a migraine usually homonymous; very rich, moving;often black and white, scintillaiton, shimmering, jagged edges headache, unilateral finger numbness and perioral numbness, vertiginous symptoms none
Occipital Seizures Bilateral minutes to hours positive, visual phenomena none, some associated with seizures
Optic Disc Drusen Unilateral/Bilateral seconds to minutes none may be entire visual field darkening or a portion of the visual field none none
Optic Disc Edema Unilateral/Bilateral seconds orthostatic changes in posture graying out, some report flashes headaches, nausea, vomiting, light sensitivty, oulsatile tinnitus, neck and back pain none
Optic Nerve Sheath Meningiomas / Orbital mass Unilateral seconds to a minute extreme gaze may be entire visual field darkening or a portion of the visual field diplopia on extreme gaze none
Orbital Emphysema Unilateral/Bilateral minutes coughing, sneezing, vomiting, Valsalva may be entire visual field darkening or a portion of the visual field orbital pain none
Retinal Emboli Unilateral 1-15 minutes coughing, bending over may be entire visual field darkening or a portion of the visual field (e.g. altitudinal visual field loss) may experience TIA none
Retinal Vasospasm Bilateral 10-20min up to an hour none may be partial or complete loss migrainous headache none
Transient Ischemic Attack Bilateral/Unilateral seconds to minutes none negative(hemianopia or blindess) brow headache, vertigo, diziness, imbalance, diplopia, bilateral weakness none
Uhthoff's Phenomenon Unilateral several minutes activities that raise core body temperature (exercise, hot tub, hot shower, outdoor activites on a hot day) difuse darkening or blurring of vision may experience paresthesias at the same time none
Uveitis-glaucoma-hyphema (UGH) Syndrome Unilateral hours to a day no particular activity, sometimes eye rubbing or fast eye movements diffuse white haze pain, if IOP is also elevated, glare none
Venous Stasis Retinopathy Unilateral seconds to minutes coughing, orthostatic positional changes usually central in retinal area supplied by cilioretinal artery none none

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Class Cases

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Referral Reason: Link Wrap-Up
80-year-old white female that has noticed repeated episodes of sudden darkening of vision. Start 31921374-Commentary
Bilateral Transient Visual Loss Start 31921375-Commentary
64-year-old women who has been experiencing episodes of haziness in vision Start 31921376-Commentary
41-year-old woman has had two episodes transient vision loss. Start 31921377-Commentary
26-year-old male was taken to the emergency room after being involved in a motor vehicle accident with subsequent transient visual loss. Start 31921378-Commentary
72-year-old with 4 episodes of vision loss. Start 31921379-Commentary

Class Survey