Mechanisms of Transient Visual Loss - Monocular

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1. Decrease in ocular perfusion pressure
1. Fixed arterial stenosis with drop in blood pressure
2. Vascular occlusive disease (giant cell arteritis) with drop in blood pressure
3. Severe transient hypotension (orthostatic or heart dysrhythmia)
4. Vasospasm of central retinal artery
5. Venous stasis retinopathy with cilioretinal artery hypoperfusion and drops in BP
6. 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, orbital air,
4. Uthoff’s phenomenon (e.g. after demyelination)
5. Hyphema – uveitis-glaucoma-hyphema (UGH) syndrome

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

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1. Decrease in ocular perfusion pressure – transient hypotension
2. Decrease in visual cortex occipital pole perfusion pressure – transient hypotension
3. Migraine – usually white out of vision or positive visual phenomena, often homonymous but the patient thinks it is one eye (e.g. right eye transient vision loss may be right homonymous phenomena)
4. Occipital seizure – usually positive visual phenomena but may be negative if post-ictal

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

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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.

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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)

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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)

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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

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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

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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