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(See also Retinal Disorders.)
Ischemic optic
neuropathy is infarction of the optic disk. The only constant symptom
is painless vision loss. Diagnosis is clinical. Treatment is ineffective.
Two varieties of optic nerve infarction exist, nonarteritic and arteritic. The nonarteritic variant occurs more frequently, typically affecting people around 50 yr and older. Vision loss tends not to be as severe as in the arteritic variant, which typically affects an older group, typically around 70 yr and older.
Most ischemic optic neuropathy is unilateral. Bilateral, sequential cases occur in about 20%, but bilateral simultaneous involvement is uncommon. Atherosclerotic narrowing of the posterior ciliary arteries may predispose to nonarteritic optic nerve infarction, particularly after a hypotensive episode. Any of the inflammatory arteritides, especially temporal arteritis (see Vasculitis: Giant Cell Arteritis), can precipitate the arteritic form.
Acute ischemia causes nerve edema, which further worsens ischemia. A small optic cup to optic disk ratio is a risk factor for nonarteritic ischemic optic neuropathy but not for the arteritic variety. Usually no medical condition is apparent to cause the nonarteritic variety, although diabetes and hypertension are present in some patients and are thought to be risk factors. Vision loss on awakening leads investigators to suspect nocturnal hypotension as a potential cause of the nonarteritic variety.
Symptoms and Signs
Vision loss with both varieties is typically rapid (over minutes, hours, or days) and painless. Some patients notice the loss on awakening. Symptoms such as general malaise, muscle aches and pains, headaches over the temple, pain when combing hair, jaw claudication, and tenderness over the temporal artery may be present with temporal arteritis; however, such symptoms may not occur until after vision is lost. Visual acuity is reduced, and an afferent pupillary defect is present. The optic disk is swollen with surrounding hemorrhages. Visual field examination often shows a defect in the inferior and central visual fields.
Diagnosis
Diagnosis is mainly based on a clinical evaluation, but ancillary testing may be needed. The most important aspect of the evaluation is to exclude the arteritic variety, because the other eye is at risk if treatment is not started quickly. ESR is usually dramatically elevated in the arteritic variety and is normal in the nonarteritic variety. C-reactive protein is also a useful monitoring test. If temporal arteritis is suspected, temporal artery biopsy should be done. For isolated cases of progressive vision loss, CT or MRI should be done to rule out compressive lesions.
Prognosis
There is no effective treatment, and most lost vision is not recovered; however, in the nonarteritic variety, up to 40% of patients spontaneously recover some useful vision.
Treatment
The arteritic variety is treated with oral corticosteroids ( prednisone 80 mg po once/day and tapered against ESR) to protect the other eye. Treatment should not be delayed while awaiting biopsy results. Treatment of the nonarteritic variety with aspirin or corticosteroids has not been helpful. Risk factors are controlled. Low-vision aids (eg, magnifiers, large-print devices, talking watches) may be helpful in both types.
Last full review/revision July 2008 by James Garrity, MD
Content last modified July 2008
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