Determine cause of transient visual loss with thorough questioning

Issue: May 2005

ByLeonid Skorin Jr., OD, DO, MS, FAAO, FAOCO

Spotlight on Prevention & Systemic Care [logo] The word “transient” may be defined as being temporary or momentary. Transient visual loss is a reversible symptom of a number of possible underlying diseases.

It can be defined by its clinical features: monocular vs. binocular, rate of onset and rate of return of vision, complete loss of vision vs. partial loss, complete visual field involvement vs. partial involvement and whether any accompanying constellation of symptoms were present during the vision loss.

Unfortunately, the underlying pathology may be difficult to establish, and, on occasion, the diagnosis cannot be confirmed or rejected by any objective test or procedure. The event is defined by the patient with additional details obtained by thorough and pertinent clinical questioning.

Patients often misinterpret whether they had a loss of vision in only one eye. This is even more evident in those who have only transient events. Occurrences of visual loss involving one hemifield will often lead the patient to believe that he or she lost vision only in the eye that had the temporal field involved.

Having the patient describe in detail what he or she could and could not visualize during the attack can help in the diagnosis. If the patient describes being able to see only half of a clock dial or half of his or her spouse’s face, then a binocular hemifield loss and not a monocular loss should be suspected.

Non-neurologic etiologies

Not all episodes of transient visual loss are due to an underlying neurologic etiology. Disturbances in the tear film often cause intermittent visual degradation. Any disruption of the corneal surface, such as corneal desiccation, abrasion or edema, can affect vision. Temporary corneal swelling from intermittent episodes of elevated intraocular pressure, such as seen in pigmentary dispersion syndrome, should always be entertained in young, active individuals. Unstable lenses or intraocular implants can move in and out of a patient’s visual axis. Opacities of the vitreal gel can obstruct vision transiently.

The three most common neurologic etiologies of transient visual loss are amaurosis fugax, classic migraine (migraine with aura) and transient visual obscurations.

Amaurosis fugax

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Amaurosis fugax is a painless unilateral loss of vision lasting from 2 to 30 minutes and followed by a total recovery. It is often described by the patient as a curtain of darkness descending over the eye. The visual loss may be complete. Recovery is in the same pattern as the initial loss. The curtain appears to rise or resolve like a clearing fog, and the vision returns to baseline levels. This recovery is usually more gradual than the vision loss progression. Because of the sudden and painless nature of amaurosis fugax, most clinicians associate it with a vascular etiology.

Another term, transient monocular visual loss (TMVL) or transient monocular blindness, is often used interchangeably with amaurosis fugax. It also describes a temporary, instantaneous unilateral complete vision loss. It has been suggested that TMVL be used to describe more prolonged episodes of loss.

Although it certainly can encompass amaurosis fugax, TMVL can also be used in a broader context. When a differentiation between these terms needs to be made, amaurosis fugax should be considered a distinct subset of TMVL caused specifically by retinal ischemia and often found to have ipsilateral retinal microemboli and ipsilateral atheromatous carotid artery obstruction.

Furthermore, both amaurosis fugax and TMVL can be presentations of a wider spectrum of disease, specifically transient ischemic attack (TIA) and reversible ischemic neurologic deficit (RIND).

TIA is a focal neurologic deficit secondary to localized ischemia lasting less than 24 hours. These patients will often have symptoms and signs in addition to the visual loss. These may include hemiparesis, hemisensory deficit, speech impediments, vertigo, ataxia, nausea, vomiting and possibly headache.

RIND is a TIA that lasts longer than 24 hours, but the patient then recovers fully within 3 or 4 weeks. These RIND episodes are also known as protracted TIAs or minor ischemic stroke. It has been found that patients with either a TIA or RIND share similar vascular risk factors and a similar prognosis. Patients whose deficits last beyond these time frames are considered to have had a disabling stroke.

Classic migraine

Auras are neurologic events seen in patients with classic migraine. Auras usually develop abruptly over 5 to 20 minutes and last less than 1 hour. In these patients, as the aura resolves, the headache usually begins. The most common type of aura appears to be visual in nature. Visual auras can be divided into types: positive phenomena or negative phenomena.

The simplest types of positive visual auras are photopsias, which are white or colored geometric figures that consist of small dots or spots, sparks, unformed flashes of light, streaks of light or wavy lines. These photopsias frequently flicker, glisten, sparkle or shimmer.

The most characteristic visual aura is the fortification spectrum, which is a formation of dazzling zigzag lines. This scintillating scotoma usually begins in the center of the visual field with an ill-defined loss of vision lined on one side with a luminous fortification spectrum. It often resembles a crescent or horseshoe-shaped visual defect bordered by moving and shining streaks of light. This scintillating scotoma often enlarges as it expands or marches to the periphery. This expansion lasts from 10 to 30 minutes and is known as the “buildup.” It usually leaves an area of impaired or obscured vision behind it.

Complex positive visual auras can include macrosomatognosia and microsomatognosia – perceptions that a part of the body is disproportionately large or small. Other positive complex phenomena include micropsias and macropsias (objects appear smaller or larger) or telopsias (objects perceived as being further away). These complex positive visual auras have been called the “Alice in Wonderland” syndrome.

Negative visual auras can also occur in patients with classic migraine. These scotomas may take the form of homonymous hemianopic or quadrantic field defects, central scotomas, tunnel vision, altitudinal visual field defects or complete bilateral blindness. Most of these scotomas are patchy and have irregular borders; therefore, patients will describe their vision as being blurred, opaque or foggy as if they are viewing objects through a film of water or heated air.

Patients with transient visual loss from migraine are usually younger and generally do not have vasculopathic risk factors such as diabetes, hypertension, cardiac or carotid disease as compared to patients with amaurosis fugax. This, in addition to the different time frames of vision loss, help make the distinction between these two illnesses.

Transient visual obscurations

The final major neurologic presentations of transient visual loss are transient visual obscurations. These are grey-outs, black-outs or blur-outs of vision lasting only 5 to 15 seconds. They may be monocular or binocular. They are often aggravated by postural changes. A patient may experience only a few of these episodes per day or may have hundreds of them, leading to functional visual incapacitation.

They are always painless. They are associated with papilledema as seen in patients with elevated intracranial pressure from a brain tumor or pseudotumor cerebri, optic nerve head drusen and in patients with anomalous discs. The brevity of transient visual obscurations distinguishes them from amaurosis fugax and migraine aura.

For Your Information:

Leonid Skorin Jr., OD, DO, FAAO, FAOCO, practices in Albert Lea, Minn., and writes and lectures on ocular disease and neuro-ophthalmic disorders. He underwent fellowship training in neuro-ophthalmology. He may be contacted at the Albert Lea Eye Clinic, Mayo Health System, 1206 W. Front St., Albert Lea, MN 56007; (507) 373-8214; fax: (507) 373-2819; e-mail: skorin.leonid@mayo.edu.