This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Recent studies have clarified the diagnosis, pathophysiology, natural history, and treatment of several diseases affecting the optic nerve. As is fitting for neurologic diseases at the turn of the twenty-first century, the information was obtained predominantly through large randomized, controlled trials and by modern molecular genetic analysis. However, the pathologic processes reflect historically standard mechanisms of disease: vascular, inflammatory, toxic/nutritional, and hereditary.
Anterior ischemic optic neuropathy.
Anterior ischemic optic neuropathy (AION) results from acute ischemia to the anterior portion of the optic nerve. [1-3] It is the most common cause of acute optic neuropathy in the elderly, frequently resulting in substantial visual dysfunction. [1-4] The patient is typically over 50 years of age and presents with sudden, painless monocular visual loss that may progress over several hours or days. As with any unilateral optic neuropathy, there should be a relative afferent pupillary defect. Swelling of the optic disc is a necessary sign for diagnosis of AION. Although many different systemic diseases have been associated with AION, the crucial initial diagnostic step is differentiating arteritic AION, that is caused by giant cell arteritis (GCA), from nonarteritic AION.
AION is the most common ophthalmic manifestation of GCA. In the patient with AION, suspicion for GCA is raised by older age, the presence of systemic symptoms such as headache, scalp tenderness, jaw claudication, muscle aches, fatigue, and weight loss, and premonitory visual symptoms such as transient monocular visual loss or diplopia. Features of AION suggestive of an arteritic etiology include early massive visual loss, chalky-white optic disc swelling, bilateral involvement, and concurrent signs of retinal circulation ischemia, such as cotton-wool spots or retinal infarction. Ancillary testing suggestive of GCA includes an elevated erythrocyte sedimentation rate and delayed or absent filling of the choroidal circulation on fluorescein fundus angiography. [5,6] The natural history of AION in the patient …
AAN Members
We have changed the login procedure to improve access between AAN.com and the Neurology journals. If you are experiencing issues, please log out of AAN.com and clear history and cookies. (For instructions by browser, please click the instruction pages below). After clearing, choose preferred Journal and select login for AAN Members. You will be redirected to a login page where you can log in with your AAN ID number and password. When you are returned to the Journal, your name should appear at the top right of the page.
AAN Non-Member Subscribers
Purchase access
Letters: Rapid online correspondence
REQUIREMENTS
You must ensure that your Disclosures have been updated within the previous six months. Please go to our Submission Site to add or update your Disclosure information.
Your co-authors must send a completed Publishing Agreement Form to Neurology Staff (not necessary for the lead/corresponding author as the form below will suffice) before you upload your comment.
If you are responding to a comment that was written about an article you originally authored:
You (and co-authors) do not need to fill out forms or check disclosures as author forms are still valid
and apply to letter.
Submission specifications:
- Submissions must be < 200 words with < 5 references. Reference 1 must be the article on which you are commenting.
- Submissions should not have more than 5 authors. (Exception: original author replies can include all original authors of the article)
- Submit only on articles published within 6 months of issue date.
- Do not be redundant. Read any comments already posted on the article prior to submission.
- Submitted comments are subject to editing and editor review prior to posting.
