Anterior ischemic optic neuropathy
From Wikipedia, the free encyclopedia
| Anterior ischemic optic neuropathy Classification and external resources |
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| ICD-9 | 377.41 |
|---|---|
| OMIM | 258660 |
| DiseasesDB | 31309 |
| eMedicine | oph/161 |
Anterior ischemic optic neuropathy (AION) is a medical condition involving loss of vision due to damage to the optic nerve from insufficient blood supply. AION is generally divided into two types: arteritic AION (or AAION) and non-arteritic AION (NAION or simply AION). This article will focus primarily on non-arteritic AION.
Contents |
[edit] Introduction
The distinction between AAION and NAION was made to highlight the different etiologies of anterior ischemic optic neuropathy. AAION is due to temporal arteritis (also called giant cell arteritis), an inflammatory disease of big-sized blood vessels (Chapel-Hill-Conference) that occurs especially with advancing age. In contrast, NAION results from the coincidence of cardiovascular risk factors in a patient with "crowded" optic discs. Non-arteritic AION is more common than AAION and usually occurs in a slightly younger group than AAION. While only a few cases of NAION result in near total loss of vision, most cases of AAION involve nearly complete vision loss.
Beyond this introduction, this article will focus on non-arteritic AION. For a discussion on arteritic AION see the separate article arteritic anterior ischemic optic neuropathy. Though the term "AION" can be used to describe either anterior ischemic optic neuropathy in general or non-arteritic AION specifically, in this article "NAION" henceforth will be used to refer to non-arteritic anterior ischemic optic neuropathy. Nonarteritic anterior ischemic optic neuropathy (NAION) is an isolated white-matter stroke of the optic nerve (ON). Nonarteritic anterior ischemic optic neuropathy (NAION) is an optic nerve stroke. NAION is the most common cause of sudden optic nerve-related vision loss, affecting more than 10,000 Americans every year, often bilaterally. No clinically effective treatments exist, largely because little is known about its pathophysiology, and there are few histopathological studies of the acute condition.[1]
[edit] Symptoms and diagnosis
NAION typically presents suddenly and upon awakening. The patient notes seeing poorly in one eye. Vision in that eye is obscured by a dark shadow, often involving just the upper or lower half of vision. There is no pain. In approximately 6-months following the infarct visual acuity improves by 3 or more lines in 42.7% of patients. In addition, vision had worsened by 3 lines or more in 12.4% of patients. Second eye involvement occurs in approximately 15% to 20% of patients with NAION within 5 years[2]. Fortunately, it may not be terribly devastating as the visual acuity may remain only moderately impaired. Furthermore, most cases of NAION involve the loss of a hemifield (either the upper or lower half of the visual field, but not both). A few cases of NAION involve almost total loss of vision.
Since arteritic NAION is similar in presentation to non-arteritic AION, patients over the age of 50 diagnosed with NAION must be evaluated to exclude AAION (symptoms: painful jaw muscle spasms, scalp tenderness, unintentional weight loss, fatigue, myalgias and loss of appetite). Furthermore, NAION patients over the age of 75 should often be blood tested regardless.
[edit] Incidence
It is estimated that the incidence of AION is about 8,000/year in the U.S.[3]
[edit] Causes and risk factors
The mechanism of injury for NAION used to be quite controversial. However, the experts in the field (neuro-ophthalmologists) have come to a consensus that most cases involve two main risk factors. The first is a predisposition in the form of a type of optic disc shape. The optic disc is where the axons from the retinal ganglion cells collect into the optic nerve. The optic nerve is the bundle of axons that carry the visual signals from the eye to the brain. This optic nerve must penetrate through the wall of the eye, and the hole to accommodate this is usually 20-30% larger than the nerve diameter called the cup to disc ratio. Hence there is extra space that acts as a margin of error. But some patients have no such margin, . Their optic disc appears "crowded" when seen by ophthalmoscopy. Nonetheless, most patients with this optic disc shape see well all of their lives.
The second major risk factor involves more general cardiovascular risk factors. The most common are diabetes, hypertension and high cholesterol levels. In patients with "a disc at risk", these vascular risk factors lead to ischemia (poor blood supply) to a portion of the optic disc. The disc then swells, but the crowded conditions don't allow space for this, so compression occurs and this leads to more ischemia. Since both eyes tend to have a similar shape, the optometrist or ophthalmologist will look at the good eye to assess the anatomical predisposition.
There is evidence that genetic factors may play a role in NAION. (see the OMIM link)
A number of studies have linked Viagra use with NAION.[4][5][6][7][8][9]
[edit] Treatment
Once NAION happens, there is no accepted treatment to reverse the damage, but prevention of further damage may be possible. Common sense dictates trying to control the cardiovascular risk factors for many reasons, including protection from this happening to the second eye. Sudden vision loss should lead to an ophthalmological consultation. If NAION is suspected, then ideally a neuro-ophthalmologist's consultation should be obtained.
There is much research currently underway looking at ways to protect the nerve (neuroprotection) or even regenerate new fibers within the optic nerve.[10][11][12][13][14] There are no current clinical trials for the treatment of NAION.
[edit] References
- ^ The morphology of an infarct in nonarteritic anterior ischemic optic neuropathy Pages 2031-2035 Rachel A. Tesser, Eric R. Niendorf and Leonard A. Levin http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6VT2-49SF08Y-10-9&_cdi=6278&_user=2854086&_orig=browse&_coverDate=10%2F31%2F2003&_sk=998899989&view=c&wchp=dGLbVlb-zSkzS&md5=fb3917c1240af40333cd77deb8a4adf9&ie=/sdarticle.pdf
- ^ IONDT(The Ischemic Optic Neuropathy Decompression Trial) Study
- ^ Hattenhauer MG, Leavitt JA, Hodge DO, et al. Incidence of nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol (United States), Jan 1997, 123(1) p103-7
- ^ Pomeranz HD, Bhavsar AR. "Nonarteritic ischemic optic neuropathy developing soon after use of sildenafil (viagra): a report of seven new cases." J Neuroophthalmol. 2005 Mar;25(1):9-13. PMID 15756125.
- ^ Egan R, Pomeranz H. "Sildenafil (Viagra) associated anterior ischemic optic neuropathy." Arch Ophthalmol. 2000 Feb;118(2):291-2. PMID 10676804.
- ^ Pomeranz HD, Smith KH, Hart WM Jr, Egan RA. "Sildenafil-associated nonarteritic anterior ischemic optic neuropathy." Ophthalmology. 2002 Mar;109(3):584-7. PMID 11874765.
- ^ Cunningham AV, Smith KH. "Anterior ischemic optic neuropathy associated with viagra." J Neuroophthalmol. 2001 Mar;21(1):22-5. PMID 11315976.
- ^ Boshier A, Pambakian N, Shakir SA. "A case of nonarteritic ischemic optic neuropathy (NAION) in a male patient taking sildenafil." Int J Clin Pharmacol Ther. 2002 Sep;40(9):422-3. PMID 12358159.
- ^ Akash R, Hrishikesh D, Amith P, Sabah S. "Case report: association of combined nonarteritic anterior ischemic optic neuropathy (NAION) and obstruction of cilioretinal artery with overdose of Viagra." J Ocul Pharmacol Ther. 2005 Aug;21(4):315-7. PMID 16117695.
- ^ Bernstein SL, Guo Y, Kelman SE, Flower RW, Johnson MA. Functional and cellular responses in a novel rodent model of anterior ischemic optic neuropathy. Invest Ophthalmol Vis Sci 2003; 44(10):4153-4162.
- ^ Bernstein SL, Guo Y, Slater BJ, Puche A, Kelman SE. Neuron stress and loss following rodent anterior ischemic optic neuropathy in double reporter transgenic mice. Invest Ophthalmol Vis Sci 2007; 48:2304-2310.
- ^ Bernstein SL, Koo JH, Slater BJ, Guo Y, Margolis FL. Analysis of optic nerve stroke by retinal Bex expression. Mol Vis 12, 147-155. 2006.
- ^ Goldenberg-Cohen N, Guo Y, Margolis FL, Miller NM, Cohen Y, Bernstein SL. Oligodendrocyte Dysfunction Following Induction of Experimental Anterior Optic Nerve Ischemia. Invest Ophthalmol Vis Sci 46, 2716-2725. 2005.
- ^ Bernstein SL, Mehrabian Z, Guo Y, Moianie N. Estrogen is not neuroprotective in a rodent model of optic nerve stroke. Molecular Vision 2007; 13:1920-1925.
[edit] External links
- Online handbook of Ocular Disease Management at revoptom.com
- Department of Ophthalmology & Visual Sciences at University of Iowa
- Polymyalgia rheumatica article from National Institute of Arthritis and Musculoskeletal and Skin Diseases
