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December 1995
Jacqueline M.S. Winterkorn, PhD, MD Great Neck, NY
A week before Christmas 1993, a 73-year-old woman sought neuro-ophthalmic consultation within hours after her discharge from a nearby hospital. She had undergone a two-week work-up at the hospital for headache and dizziness. She'd been told the diagnosis was hypertension.
During hospitalization, she had complained of blurred vision, but the CT-scan was negative, and a confrontation visual field examination by a neurologist (using wiggling fingers) failed to reveal a visual field defect. The neurologist told her to see an ophthalmologist for "glasses" after discharge.
The neuro-ophthalmic exam revealed decreased acuity in the left eye, and a central retinal artery occlusion. A left hemianopic visual field defect was apparent in both eyes, confirmed with a 24-2 threshold test (Fig. 1). How would you have worked up this patient?
The standard approach to the evaluation of ocular and cerebral vascular obstruction is to "round up the usual suspects." Physicians routinely order a costly battery of neuroimaging tests, including MRI, MRA, duplex scanning, transcranial Doppler, echocardiography (especially transesophageal echocardiogram) and blood tests for hypercoagulability (see box).
In this case, however, we reasoned that a left CRAO implicated the left anterior circulation, while a left homonymous hemianopsia implicated the right posterior (vertebrobasilar-posterior cerebral) circulation. The co-occurrence of both suggested that the source was either the heart or a systemic process. Transesophageal echocardiography, done that afternoon, revealed an embolic source from a clot in the atrial appendage, where poor movement promoted stasis. The patient was heparinized, then started on . By Christmas, she was home and out of danger.
Careful history and examination of the patient who has experienced visual loss often can suggest the source of the problem, direct and streamline further evaluation, prevent indiscriminate testing, and determine the correct etiologic diagnosis and appropriate treatment efficiently and economically. Permanent visual loss can sometimes be preceded by transient visual loss. Common causes of transient visual loss include:
Embolism is a common cause of cerebral or retinal vascular obstruction leading to visual loss.
Patients often report episodes of transient visual loss or dimming before losing vision permanently.
It is important to consider that transient visual loss can result from pathology affecting one eye, or from pathology affecting one half of the visual field in both eyes. Patients unfamiliar with the anatomy of the visual system usually report the problem in one eye even when they have actually experienced an homonymous hemianopsia. With clues from history and careful physical examination, the ophthalmologist may be able to locate the defect nevertheless.
Amaurosis fugax, from the Latin for fleeting blindness, is much less common than homonymous hemianopic loss. Monocular vision loss tends to be brief, lasting only seconds to minutes, whereas binocular homonymous hemianopsia may last for 20 to 30 minutes before resolving. Unlike binocular defects, which patients recognize with both eyes open or closed, amaurosis fugax typically can only be appreciated if the patient covers the good eye. For this reason, it often goes unnoticed.
Emboli in the retinal circulation are the most important cause of amaurosis fugax. The patient who has experienced retinal vascular obstruction typically reports that a "curtain of darkness" descends over the eye. In cases where some residual circulation persists, the vision may only be partially obscured. When the embolus dissolves or moves on, the curtain appears to rise or resolve like a clearing fog, and vision returns.
Sometimes, emboli do not obstruct blood flow even transiently, but still cause symptoms. In such cases, patients report brief photopsias, or swirling points of light. The patient may acknowledge seeing tiny spots of light that appear temporally (indicating emboli emerging from the central retinal artery on the disc), travel jerkily across the visual field (as the emboli pulse through the retinal circulation from bifurcation to bifurcation) and then disappear.
Rarely, it is possible to see emboli passing through the retinal vessels by funduscopy. When infarction occurs, a cotton-wool spot develops over the next day.
When the embolus is visible, it's possible to infer the source from its appearance.
Cholesterol emboli, or Hollenhorst plaques, appear as shiny, golden crystals. They usually represent embolization from the carotid arteries. There may be more than one. They usually lodge at vessel bifurcations. Although they seem larger than the vessel they occupy, they often do not block blood flow, and the blood column will be visible distal to the plaque. When the ophthalmologist applies pressure to the globe during ophthalmoscopy, the cholesterol shard may rock with the pulse or even dislodge and move on.
Calcific emboli appear as grey-white blobs at or near the optic disc. They originate from cardiac valvular lesions. They most often result in complete obstruction of the involved vessel, leading to retinal infarction and permanent, rather than transient, visual loss. Such emboli may remain in place for years, and occasionally, a collateral vessel may eventually bypass the obstruction. One of my patients, who had a history of rheumatic heart disease, suffered calcific emboli in each eye and developed collateral shunting bilaterally. Her fundi are depicted on the cover and inside the November 1995 Archives of Ophthalmology.2
Fibrin-platelet emboli are almost never present at the time of funduscopy, but have been described as cream-colored elongated plugs filling the vessel. These represent platelets and associated thrombotic material combining at sites of intravascular irregularity, especially in patients with hypercoagulable tendencies. Since these emboli usually dissolve and are carried away before they can be observed by a physician, vascular sheathing may be the only clue to their prior passage.
Although patients with embolic disease are at high risk for stroke, and may require extensive evaluation of heart and great vessels, the likely source of an embolus may also be predicted by the patient's age and medical history. For example, a patient under 40 is unlikely to have carotid artery disease, and more likely to have a cardiac source, particularly if there is a history of cardiac valvular disease or use of illicit drugs.
Seven years ago, a 56-year-old man who had suffered a branch retinal artery occlusion in the left eye visited my office for an evaluation prior to a left carotid endarterectomy. Since he described amaurotic episodes in both eyes, and his retinal exam suggested the recent passage of thrombin platelet emboli in both eyes, a unilateral endarterectomy did not seem like the correct therapy! Surgery was cancelled and blood tests revealed a lupus-like anticoagulant. Over the years, he has remained well on a regimen that includes aspirin, and a calcium channel blocker. Although he continues to have occasional visual symptoms, he never again suffered a retinal or cerebral infarction.
This occurs in patients with critical carotid stenosis, cardiac arrhythmias, elevated intraocular pressure, or increased intracranial pressure. Such patients describe progressive dimming or shrinking of the field of vision from the periphery inward, lasting as briefly as a few seconds. Transient visual obscurations may be positional, occuring when the patient sits up after lying flat, or stands up after bending over.
Ophthalmologists must consider this possibility early in the differential diagnosis of any elderly patient with transient visual loss. It represents one of the few true ocular emergencies, since if it is not treated immediately and aggressively, it can progress rapidly to bilateral blindness from arterial occlusion or ischemic optic neuropathy.
Ask the patient about symptoms such as headache, pre-auricular pain when chewing, scalp soreness, muscle and joint pain, appetite depression and weight loss.
Diplopia can be the presenting symptom when arteritis produces vascular occlusion in extraocular muscles, mimicking vasculopathic VIth nerve and partial IIIrd nerve pareses.
Physicians should obtain a Westergren erythrocyte sedimentation rate (WESR) along with a complete blood count (CBC). The C-Reactive Protein test can help confirm the diagnosis. Anemia and a high WESR are useful in diagnosis, but the WESR may not be extremely elevated early, so maintain a high level of suspicion in the presence of any elevation over past levels. Begin prompt treatment with high-dose oral or intravenous steroids to prevent visual loss. If the patient has lost vision in one eye, immediate intravenous therapy may still allow some recovery.
Since prolonged steroid therapy, especially in the elderly, carries with it the danger of fungal and other opportunistic infections, bleeding ulcer, muscle wasting, and diabetic complications, a temporal artery biopsy must be obtained at the earliest convenience to confirm the diagnosis.
In one case, a healthy athletic 70-year-old man wintering in Florida thought he had caught the "flu." His wife had to help him dress in the morning because of the pain he experienced when his undershirt touched his tender scalp. He complained to his internist of myalgias, weakness, and "sinus" headaches. The internist arranged an otorhinolaryngologic consultation. Despite an unremarkable CT-scan, a WESR level of 127, and a symptom of pain in front of his ear when he chewed, the patient was admitted to a hospital for a sinus procedure. Shortly after the procedure, the patient complained to a nurse that he saw a "tree" in front of his left eye. An ophthalmologist was summoned, but he did not inquire about the patient's symptoms and the patient did not bring them up; he said later that he was too tired and depressed. The ophthalmologist found a normal visual acuity and normal intraocular pressure, and attributed the disc swelling he observed to post-sinusitis inflammation. He suggested that the patient consult with him again during the following week.
On the way home from the hospital the next day, the patient lost sight first in the left and, within 15 minutes, in the right eye. By the time he arrived home, he was bilaterally blind. Despite subsequent treatment with high-dose intravenous steroids, the patient's sight never improved beyond finger counting. The temporal artery biopsy was positive for temporal arteritis.
This condition in the ophthalmic or retinal artery has recently been accepted as an important cause of transient monocular visual loss, especially in young patients with automimmune diatheses and in elderly patients with atherosclerosis. In such patients the attacks of amaurosis fugax may be frequent, lengthy, and unresponsive to aspirin. Nevertheless, vasospasm remains a diagnosis of exclusion. The work-up must include cardiac and carotid evaluation, and blood tests for hypercoagulability and hyperviscosity syndromes, such as WESR, CBC, anticardiolipin antibody, antiphosphotidyl choline and antiphosphotidyl serine, PTT, VDRL, Protein C, Protein S, and resistance to activated Protein C and Plasminogen. When other causes have been ruled out, calcium channel blockers such as Nifedipine or Verapamil may be effective.3,4
Binocular, homonymous hemianopic visual loss occurs much more commonly than true amaurosis fugax, although patients may not recognize its binocularity. The most common causes of such defects are cortical migraine in the young, and "late-life migraine," which represents occipital ischemia, in the elderly.
Classical cortical migraine is characterized by a visual aura preceding a sick headache and may affect 20 percent of the population, women more frequently than men. The headaches usually commence when the patient is in her teens or twenties. There often is a strong family history, and many migraineurs report having experienced motion sickness in childhood.
The typical visual aura includes scintillating lights, colors, and zig-zag lines. These lines, often compared to medieval "fortifications" or to cartoon lightning, indicate a cerebral, not retinal location, since they probably correspond to cortical orientation columns.
The characteristic migrainous teichopsia is a hallucination beginning as a small C-shaped form, with its open side toward the midline. This form gradually expands and moves laterally over about 20 minutes until it disappears in the periphery. The C-shaped figure is a focus of positive phenomena, including scintillating, many-colored zig-zag lines (see Figure 2).
The positive phenomena may be followed by a period of visual field depression, even a complete homonymous hemianopsia. When headache occurs, it usually begins as the visual aura is resolving. Especially in young patients, the headache may be exquisitely painful, hemicranial, and accompanied by nausea, vomiting and sensitivity to light and sound. Some patients suffer the headache for days, with no relief even during sleep. Other patients, especially the elderly, may experience "acephalgic migraine," consisting of the visual aura without subsequent pain. Acephalgic migraine occurring for the first time in an elderly patient heralds vertebrobasilar insufficiency. Although the visual loss may be frightening to the patient, the prognosis for retaining vision is usually good with aspirin prophylaxis.
A migraine may not require any workup. However, when a migrainous aura lasts longer than an hour, follows rather than precedes headache, occurs repeatedly on one side only, or is associated with a fixed scotoma, pursue further evaluation to rule out a tumor (such as an occipital meningioma) or a completed stroke.
Sudden visual loss is a serious symptom which can indicate impending morbidity or even mortality. Thoughtful analysis after a careful history and examination can play a significant part in ensuring a good outcome.
Dr. Winterkorn, who is in private practice, is an Associate Professor of Ophthalmology and of Neurology and Neuroscience at Cornell University Medical College.
References:
1. Winterkorn, JMS, Odell, JG. Neuro-ophthalmic clues to systemic disease, in Neuro-Ophthalmoloy, Burde R and Slamovits T (eds) of Yanoff and Podos Textbook of Ophthalmology, Mosby Press, !994.
2. Winterkorn, JMS, Ptachevich, Y: Calcific Retinal Emboli and Collateral Shunting in a Woman with Rheumatic Heart Disease. Arch Ophthalmol, Vol. 113, Nov. 1995, p. 1464-5.
3. Winterkorn JMS, Kupersmith MJ, Wirtschafter JD, Forman S. Treatment of vasospastic amaurosis fugax with calcium-channel blockers. N Eng J Med 1993;329:396-398.
4. Winterkorn, JMS, Teman, AJ. Recurrent attacks of amaurosis fugax treated with calcium channel blocker. Annals of Neurol, Vol. 30, 423-425, 1991.
Sometimes, the cause of transient vision loss is local to the ocular or periocular tissues. Among the possible local causes:
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