What is the focus of clinical history to evaluate transient vision loss (TVL)?

Updated: May 21, 2019
  • Author: Andrew J Tatham, MD, MBA, FRCOphth, FEBO, FRCS(Ed); Chief Editor: Andrew G Lee, MD  more...
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Answer

Answer

Because of the many causes of transient visual disturbance, a structured approach to both the assessment and the management of these patients is essential. The likely causes of transient vision loss (TVL) vary according to the age of the patient. Ischemic causes are more common in patients older than 45 years; however, cases of impending central retinal artery occlusion and central retinal vein occlusion have been reported in children. [30]

Perhaps the most important element to ascertain from the history is whether the visual disturbance is monocular or binocular. [31, 32] A monocular visual disturbance is more likely to be secondary to a circulatory disturbance of the anterior circulation (eg, carotid artery) than a binocular visual disturbance, which is often due to a disturbance of the posterior circulation (eg, vertebral or basilar artery). Unfortunately, patients, particularly children, often have difficulty distinguishing between monocular and binocular symptoms.

Transient monocular visual loss is often referred to as amaurosis fugax, irrespective of the cause. However, it is more accurate to reserve the term amaurosis fugax for episodes of transient monocular blindness resulting from ischemia of the ocular vessels. [2] A vertebrobasilar disturbance may cause a visual transient ischemic attack (TIA).

Amaurosis fugax and a visual TIA are similar in several respects: Both are of sudden onset, last 2-30 minutes, and resolve quickly without pain. Amaurosis fugax typically consists of a gray curtain that progresses from the periphery and moves toward the center of vision. It is vital to identify patients whose visual disturbance is ischemic because these patients are at greater risk for cerebrovascular accident, cerebral TIA, and myocardial infarction (MI).

The risk of further thromboembolic events is less after amaurosis fugax than after a visual TIA. [33] Repeated episodes of visual loss may be of thrombotic rather than embolic origin.

Whereas amaurosis fugax lasts only a few minutes (rarely longer), with vision returning to normal within 10-30 minutes, a migraine headache tends to last 2-3 hours (rarely more than 12 hours). The visual disturbance in migraine expands slowly over 10-20 minutes and rarely lasts more than 30 minutes.

Any precipitating factors for the visual loss should be elicited. For example, visual loss related to orthostatic changes may occur in patients with papilledema. The patient should be asked about the specific nature of the disturbance. Ischemic visual disturbances, such as amaurosis fugax, are classically associated with negative phenomena (eg, a blackout of vision or a curtain across the vision). Migraine tends to produce positive phenomena (eg, sparkling lights or zigzag lines).

Details of visual symptom progression can yield etiological information. Altitudinal visual field loss, symptoms of retinal claudication, and visual loss duration of 1-10 minutes are more indicative of carotid artery stenosis as an etiology. [34]

Associated symptoms may provide important clues to the etiology. Adults should be specifically asked about the symptoms of giant cell arteritis. Children should be asked about headaches and specifically about features of headaches that may suggest raised intracranial pressure (ICP) or migraine.

As part of the medical history, the patient’s ischemic risk factors should be assessed, including any history of hypertension, diabetes, or high cholesterol levels. Inquire about a personal history of migraine, as well as about a family history. Consider whether the patient has any systemic conditions (eg, collagen vascular disease, sickle cell disease, or vasculitis).


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