Update on the evaluation of transient vision loss

Figures & data

Table 1 Categories of transient vision loss

Location	Causes of transient vision loss
Monocular	Vascular – embolic
	Vascular – thrombotic (giant cell arteritis)
	Vascular – stenotic
	Vasospasm
	Retinal migraine
	Ocular – closed angles, hyphema
Binocular	Vascular – thromboembolic
	Occipital epilepsy
	Complex migraine
Monocular or binocular	Papilledema or optic disc disease (transient visual obscurations)
	Uhthoff phenomena

Notes: Monocular and binocular vision losses have overlapping and specific causes. Transient visual obscurations and Uhthoff phenomena are also important causes of transient vision loss, but the context of these is distinct enough from the others that we will not be highlighting them in this review.

Table 2 Patient history of transient vision loss

Questions to ask regarding transient vision loss
Monocular or binocular
Duration and timing of vision loss
Provoking factors (positional change, sexual activity)
Associated symptoms (giant cell arteritis ROS, migraine headaches)
Pattern of vision loss (altitudinal versus diffuse/constricting)
Retinal claudication
Recent ocular surgery or cerebral angiography
History of atrial fibrillation or thromboembolic disease

Notes: Certain questions may have added importance in the patient with transient vision loss. The answers can direct and focus ancillary testing to determine etiology.

Abbreviation: ROS, review of systems.

Table 3 Treatment of carotid disease after transient vision loss

Present	Three of the following other risk factors
>70% carotid stenosis	Male sex
	Lack of collaterals on angiogram
	Hemispheric transient ischemic attack (TIA)
	Peripheral vascular disease
	80%–94% carotid stenosis
	Age >75

Note: Because the North American Symptomatic Carotid Endarterectomy Trial noted a decreased risk of stroke after transient vision loss compared to other TIA presentations, it has been suggested that surgical treatment of carotid disease be restricted to patients with only a certain subset of risk factors listed here.

Table 4 Hereditable thrombophilias

Thrombophilia	Mechanism causing hypercoagulability
Methylene tetrahydrofolate reductase mutation	Causes an increase in homocysteine, an amino acid intermediate in the metabolism of methionine which is linked to thrombosis
Protein C and S deficiency	Protein S is a cofactor for protein C, which is a proteolysis enzyme of factor Va and VIIIa
Antithrombin III deficiency	Antithrombin III is a protease for most clotting factors
Factor V Leiden mutation	The mutation results in an increase in the function of factor V, causing protein C to function improperly
G20210A mutation	Mutation in the prothrombin gene resulting in elevated plasma prothrombin

Note: Both the mutation or deficiency and the mechanism causing hypercoagulability are listed here for the most commonly tested hereditable thrombophilias.