Nonarteritic anterior ischemic optic neuropathy remains a disease that is poorly understood in many aspects. The clinical presentation may diverge significantly from the classic unilateral, painless, sudden vision loss affecting patients over the age of 50 years. This variability might make nonarteritic anterior ischemic optic neuropathy hard to differentiate from optic neuritis and arteritic ischemic optic neuropathy. The course of nonarteritic anterior ischemic optic neuropathy is also variable, often sequentially affecting the other eye.
Visual recovery has been reported, but it is not the rule. Multiple risk factors have been proposed, including crowded disc, atherosclerosis, diabetes, hyperlipidemia, hypertension, hypotension, hemoconcentration, hemodilution, and hypercoagulable states. The optic nerve damage in nonarteritic anterior ischemic optic neuropathy appears to result from a perfusion insufficiency in the short posterior ciliary arteries leading to infarction of the retrolaminar portion of the optic disc. The underlying mechanisms are still unclear, however. Multiple medical and surgical treatment options have been investigated, including optic nerve sheath decompression, standard and megadose corticosteroids, levodopa, carbidopa, hyperbaric oxygen, and neuroprotective agents, but no proven effective treatment is currently available.
Intense investigations in humans and animals are under way. Hopefully these studies will enhance our understanding of the risk factors and pathophysiology of nonarteritic anterior ischemic optic neuropathy and aid in developing new strategies for prevention and treatment.
Department of Ophthalmology, University of Maryland, Baltimore, Maryland
Correspondence to Michaela Kunz Mathews, University of Maryland, Department of Ophthalmology, 419 W Redwood Street, Baltimore, MD 21201, USA
Tel: 410 328 7261; fax: 410 339 5346; e-mail: email@example.com