Ішемічна невропатія зорового нерва

Vision loss with both varieties of optic nerve infarction is typically rapid (over minutes, hours, or days) and painless. Some patients notice the loss on awakening. In arteritic ischemic optic neuropathy due to giant cell arteritis, 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 are usually present; however, such symptoms may be absent in up to 20% of cases (1). Visual acuity is usually reduced, and an afferent pupillary defect is present.

The optic disk is swollen and elevated, and the swollen nerve fibers obscure the fine surface vessels of the optic nerve. Often hemorrhages surround the optic disk. The optic disk may be pale in the arteritic variety and hyperemic in the nonarteritic variety. In both varieties, visual field examination often shows an altitudinal and/or central defect.

• Erythrocyte sedimentation rate (ESR), C-reactive protein, and complete blood count (CBC)

• Computed tomography (CT) or magnetic resonance imaging (MRI) of the brain and orbits if vision loss is progressive

Diagnosis of optic nerve infarction is based mainly on clinical evaluation, but ancillary testing may be needed. Most important is to exclude the arteritic variety because the other eye is at risk if corticosteroid treatment is not started quickly. Immediate tests include ESR, CBC, and C-reactive protein. ESR is usually elevated in the arteritic variety, often exceeding 100 mm/hour, and normal in the nonarteritic variety. C-reactive protein is also elevated and is more sensitive than ESR in diagnosing giant cell arteritis. Only 4% of biopsy proven GCA have normal values for both C-reactive protein and ESR. CBC is done to identify thrombocytosis (> 400 × 10³/mcL), which adds to the positive and negative predictive value of using ESR alone (1).

If giant cell arteritis is suspected, corticosteroids should be started immediately, and temporal artery biopsy should be done as soon as feasible (at least within 1 to 2 weeks because effects of the prednisone therapy may reduce the diagnostic yield of histopathology). Changes in C-reactive protein level are useful for monitoring disease activity and the response to treatment. For cases of progressive vision loss, CT or MRI of the brain and orbits should be done to rule out compressive lesions.

For nonarteritic ischemic optic neuropathy, additional testing may be indicated based on the suspected cause or risk factor. For example, if patients have excessive daytime sleepiness or snoring or are obese, polysomnography should be considered to diagnose obstructive sleep apnea.

• Corticosteroids and tocilizumab for the arteritic variety

The arteritic variety is treated with oral corticosteroids (prednisone 80 mg orally once a day and tapered based on erythrocyte sedimentation rate and C-reactive protein) to protect the other eye. If there is vision loss, intravenous corticosteroids should be considered. Treatment should not be delayed while awaiting the biopsy procedure or its results. Results from clinical trials show that tocilizumab given when tapering corticosteroids improves glucocorticoid-free remission when compared to corticosteroids alone in giant cell arteritis (1). There is no established treatment of the nonarteritic variety. Vascular risk factors should be optimized. Low-vision aids (eg, magnifiers, large-print devices, talking watches) may be helpful in both types.

There is no effective treatment for the nonarteritic variety of optic nerve infarction; however, up to 40% of patients have mild spontaneous recovery of vision (1).

In the arteritic variety caused by giant cell arteritis, losses of visual acuity and visual field are typically greater. Prompt treatment does not restore lost vision in the affected eye but protects the unaffected eye. Inadequate treatment risks relapses and additional vision loss.