Transient visual loss (TVL) is the sudden loss of visual function (partial or complete) in 1 or both eyes that lasts less than 24 hours. In general, the most important cause of transient monocular visual loss (TMVL) is retinal ischemia due to temporary occlusion of the central retinal artery or its branches. The most common cause of transient binocular visual disturbance is migraine. A systematic approach to the evaluation of patients with TVL is imperative, beginning with a detailed historical account of the visual loss that includes the following points:
Monocular versus binocular. Establishing TVL as monocular or binocular is important for localizing the lesion; monocular loss implies a prechiasmal problem (anywhere from the cornea to the optic nerve), whereas binocular loss is a chiasmal or retrochiasmal (intracranial) problem. In rare instances, binocular TVL can reflect bilateral ocular disorders. Patients should be asked if they occluded each eye during the episode of visual loss. Clinicians should be aware that transient homonymous hemianopia is frequently misperceived as a monocular visual loss in the eye with the temporal field deficit.
Age. In patients younger than 50 years, migraine is the most likely cause of binocular TVL. Arterial vasospasm can cause TMVL, but it is not common and is a diagnosis of exclusion. An important exception in pregnant women is eclampsia, in which TVL may be a harbinger of more serious and permanent visual loss, usually occurring within days of delivery (see Chapter 14). In older patients, cerebrovascular disease and giant cell arteritis (GCA) should be considered.
Duration of visual loss. Monocular or binocular transient obscurations of vision lasting only seconds are often precipitated by a change in posture (eg, bending over) and are a common complaint in patients with optic nerve head (ONH) drusen or papilledema. Sudden TMVL lasting several minutes (typically no more than 15 minutes) is more suggestive of retinal ischemia from emboli. The duration of visual loss from retinal artery vasospasm varies; it may last seconds to 1 hour. TMVL resulting from ocular hypoperfusion or venous insufficiency can last up to 30 minutes. Occipital seizures are very brief binocular visual disturbances that last only a few seconds, whereas the binocular scintillating scotoma typical of migraine lasts 20–30 minutes.
Pattern/description of visual loss and recovery. The classic description of TMVL from retinal emboli is a descending curtain in 1 eye; however, tunnel-like contraction of vision or sudden complete loss of vision may also occur. An altitudinal aspect of visual loss strongly suggests retinal emboli, but central retinal artery vasospasm can sometimes cause similar visual symptoms. Visual loss or disturbance precipitated by exercise can be caused by vasospasm, pigment dispersion syndrome, or demyelinating disease. Uhthoff phenomenon (transient visual blurring resulting from physical activity or elevation in body temperature) frequently occurs in patients with a current or previous episode of optic neuritis (see Chapter 4). Posterior circulation ischemia typically causes complete bilateral TVL (ie, cortical blindness) or a homonymous hemianopia, often in association with brainstem and/or cerebellar symptoms. Binocular visual disturbances with geometric quality (eg, “fortification” pattern) strongly suggest occipital lobe dysfunction (eg, migraine, ischemia, or seizure). Whiteout of vision in both eyes or gradual constriction (ie, “closing in”) of peripheral vision without positive visual phenomena may also signal occipital lobe ischemia.
Associated symptoms and additional signs. Positive visual phenomena and headache accompanying binocular TVL suggest migraine. Persistent headaches and pulsatile tinnitus suggest increased intracranial pressure. In an elderly patient, TVL accompanied by headaches, weight loss, fever, malaise, jaw claudication, and scalp tenderness strongly suggests GCA. The presence of other neurologic symptoms and signs can help localize the vascular territory involved. Loss of consciousness, dizziness, diplopia, dysarthria, or focal weakness accompanying binocular TVL suggests cerebral ischemia in the posterior circulation (basilar artery territory). Focal weakness contralateral to the TMVL or aphasia suggests cerebral ischemia in the anterior circulation (internal carotid artery territory). Ipsilateral periorbital pain in the setting of an ipsilateral Horner syndrome may indicate an internal carotid artery dissection (see Chapter 10, Fig 10-4). TVL associated with exercise or change in position may suggest hypoperfusion (eg, ocular ischemic syndrome). Skin or joint changes or Raynaud phenomenon may accompany systemic vasculitis.
Predisposing conditions. The examiner should conduct a careful interview, eliciting information about the presence of vascular risk factors such as atheromatous disease (carotid stenosis, coronary artery disease, peripheral arterial disease, aortic aneurysm), diabetes mellitus, hypertension, dyslipidemia, smoking, sleep apnea, cardiac source of emboli (previous myocardial infarction, valvulopathy, arrhythmia), intravenous drug use, family or personal history of a clotting disorder, systemic cancer, and history of connective tissue disease or vasculitis (eg, GCA or Takayasu arteritis).
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Lawlor M, Perry R, Hunt BJ, Plant GT. Strokes and vision: the management of ischemic arterial disease affecting the retina and occipital lobe. Surv Ophthalmol. 2015;60(4): 296–309.
Although the patient may report complete recovery of visual function, a thorough examination is crucial to rule out ocular and orbital causes of TVL, to assess the afferent visual function, and to look for retinovascular clues (eg, emboli, cotton-wool spots, vascular attenuation, or hemorrhage) that might suggest a specific diagnosis. This process should include testing for best-corrected visual acuity (also called corrected distance visual acuity), color vision, and intraocular pressure (IOP), as well as an examination of the pupils (testing for relative afferent pupillary defect or Horner syndrome), a slit-lamp examination, perimetry to look for residual visual field defects, and a dilated funduscopic examination. A positive photostress recovery test may indicate macular ischemia (see Chapter 3). When a vascular mechanism is suspected, retinal fluorescein angiography may be helpful.
Excerpted from BCSC 2020-2021 series: Section 5 - Neuro-Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.