Transient visual loss that has resolved by the time of presentation is often challenging to evaluate, as the examination is often normal, and both benign and dangerous etiologies are possible.
A first step is to distinguish between structures that refract and focus light (the cornea and lens) and those that sense light (retina) and carry and process visual information (optic nerves, chiasm, tracts, visual cortex). Ocular surface disease (e.g., corneal dryness, abrasions, or edema) is typically experienced as blurring, haziness, or fogging of vision without overt vision loss. Here, light reaches the retina, but the image projected on the retina is out of focus. In contrast, diseases of the retina, optic nerve, or other visual pathway structures are more likely to be experienced as darkening or loss of vision. Additionally, ocular surface disease usually results in diffuse blurring of vision. A history of distinctly focal visual symptoms such as isolated central, altitudinal, or hemianopic blurring would be atypical for ocular surface disease and increases suspicion for a neurologic process.
Uhthoff phenomenon, which refers to fluctuation of neurologic symptoms associated with changes in body temperature in patients with multiple sclerosis, was first described in optic neuritis. An increase in body temperature, such as with a hot shower or exercise, transiently decreases myelin conduction through an affected optic nerve, causing transient visual symptoms.
During eye movement, the position of the optic nerve head within the orbit shifts from one side to the other. If there is an intraorbital mass lesion, this movement may cause transient stretching and compression of the optic nerve, which may be experienced as gaze-evoked vision loss. Magnetic resonance imaging (MRI) of the orbits should be performed for evaluation.
Transient binocular vision loss can indicate simultaneous bilateral retinal or optic nerve dysfunction or unilateral or bilateral occipital lobe dysfunction. Transient visual obscurations due to papilledema are an example of the former. Retinal and optic nerve perfusion pressure is dependent on both intraocular and intracranial pressure; as either of these increase, retinal and optic nerve perfusion decreases and can be sufficiently impaired to cause transient vision loss. The same principle underlies the vision loss that is experienced during presyncope, which is thought to be due to transient bilateral retinal ischemia caused by a drop in arterial pressure. Rarely, an embolus to the distal basilar artery may obstruct flow to both posterior cerebral arteries, causing transient diffuse visual loss. There are usually other accompanying neurologic symptoms in this scenario.
When considering transient visual phenomena of cortical origin, a helpful distinction is between those that cause positive symptoms (photopsias and other visual hallucinations) and those that cause purely negative symptoms (vision loss). Positive visual phenomena are more likely to accompany migraine or occipital lobe seizures, whereas pure loss of vision is more common with occipital lobe ischemia. This distinction is not, however, completely reliable.
Retinal migraine is a rare cause of transient monocular visual phenomena, both positive and negative, and is typically associated with headache. The exact mechanism is uncertain, and the diagnosis itself as distinct from classic migraine with aura is somewhat controversial. Often there are multiple recurrent attacks. Carotid dissection can cause retinal ischemia and present with transient monocular visual loss; headache, neck pain, and an ipsilateral Horner syndrome are common symptoms of dissection. Given the risk of potentially catastrophic stroke, a high level of suspicion should exist for this entity. Diagnosis can be made with MRI or computed tomography angiography. Carotid ultrasound is not sufficient to exclude dissection, as it often affects the distal cervical carotid artery, outside the field of view of ultrasound.
Giant cell arteritis affects older patients and can cause transient retinal ischemia, though fixed deficits (ischemic optic neuropathy, retinal artery occlusion) are more common. Headache, scalp tenderness, jaw claudication, and constitutional symptoms are often present. The sedimentation rate is usually markedly elevated. Prompt administration of steroids is critical for preventing further vision loss.
The term amaurosis fugax is synonymous with a transient ischemic attack of the retina, which may be due to carotid stenosis or cardioembolism. Symptoms are often described as being similar to a shade coming down over the eye. Vascular and cardiac imaging should be performed, and appropriate antithrombotic therapy started. If high-grade atherosclerotic carotid stenosis is present, revascularization should be undertaken as soon as feasible. When multiple recurrent attacks of transient monocular visual loss occur with normal cardiac and vascular testing, vasospasm should be considered. These patients often respond to calcium channel blockers.