The anterior section of the optic nerve, which is largely supplied by the posterior ciliary artery circulation, suffers from ischemia damage, which causes anterior ischemic optic neuropathy (AION). There are two different kinds of anterior ischemic optic neuropathy: arteritic AION (AAION), which develops as a result of vasculitis, particularly giant cell arteritis, and non arteritic AION (NAION), which develops as a result of non-inflammatory small vessel disease. The most common cause of acute optic neuropathy in those over 50, NAION accounts for 95% of all instances of AION and affects 2–10 people per 100,000 people (approximately 1500 to 6000 new cases per year in the United States). 34 There isn't yet a widely acknowledged secondary preventive or treatment for NAION. We go over the methods recommended for treating NAION [1].

Non arteritic Anterior ION 

Diagnosis and Clinical Presentation: Hypoperfusion and ischemia of the anterior optic nerve are caused by small-vessel disease of the affected area. The ischemia is made worse by a series of actions, which frequently has negative effects on vision. The symptoms of nonarteritic anterior ION include isolated, abrupt, painless, monocular vision loss and optic disc edoema. It is usual for vision to gradually deteriorate over a few days or weeks, and this is probably due to growing ischemia in the context of a local compartment syndrome brought on by the disc edoema. A relative afferent pupillary deficiency and edoema of the optic disc, which is made up of the optic-nerve head, are required to support the clinical diagnosis of acute nonarteritic anterior ION.  The presence of a small, congested optic-nerve head and a small physiological cup during inspection is a significant finding; this small cup-to-disc ratio designates a "disc at risk [2]."

Examining the normal eye should reveal a disc at risk, despite the fact that this result is challenging to discern during the acute phase of nonarteritic anterior ION when the optic disc is enlarged. 

Usually, the disc edoema goes away over the course of 6 to 11 weeks, and disc pallor appears, frequently in a sectoral pattern. Patients with nonarteritic anterior ION often have normal imaging of the optic nerve. When there is clinical doubt, contrast enhanced magnetic resonance imaging (MRI) of the orbits with fat suppression is most helpful to rule out a compressive optic neuropathy or an inflammatory optic neuritis. The anterior ION must be recognized. In patients with acute optic neuropathy, inflammatory optic neuritis is frequently over diagnosed, which raises questions about multiple sclerosis and frequently has negative patient outcomes [3].

Treatment

Similar to the arteritic kind of anterior ION, there is no proven treatment for nonarteritic anterior ION. Therefore, differentiating between arteritic and nonarteritic anterior ION and identifying and managing vascular risk factors in nonarteritic anterior ION cases are the most crucial therapeutic considerations. The majority of suggested treatments for nonarteritic anterior ION are predicated on this presumptive mechanism and sequence of events. Although several treatments have been tried, few have been well researched, and animal models with nonarteritic anterior ION have just recently begun to appear. Surgery had no positive effects in the IONDT, a major, multicenter, prospective treatment study for nonarteritic anterior ION. Anti-vascular endothelial growth factor or glucocorticoid intravitreal injections are helpful at reducing disc edoema but do not appear to enhance visual outcomes. In a sizable, uncontrolled, retrospective analysis, oral glucocorticoids were found to affect visual outcomes, although the moderate potential effect must be weighed against the significant risk of glucocorticoid problems in these patients with vasculopathy, many of whom have diabetes. The efficacy of other therapies, such hyperbaric oxygen therapy, has not been established [4].

Non Arteritic Posterior Ion

The term "posterior ION" is used when the posterior section of the optic nerve is ischemic and there is no discernible disc edoema. Compared to nonarteritic anterior ION, nonarteritic posterior ION is incredibly uncommon. A relative afferent pupillary deficit, a normal appearing optic nerve head, and an isolated, painless, rapid loss of vision in one eyeare the characteristic symptoms of nonarteritic posterior ION. Four to six weeks later, optic-disc pallor appears, as is typical with any optic neuropathy. With other causes of posterior optic neuropathy (such as inflammatory and compressive causes) being ruled out by high-quality MRI of the brain and orbits with contrast and with fat suppression and by an extensive workup for underlying systemic inflammatory disorders, the diagnosis of nonarteritic posterior ION is challenging clinically and remains a diagnosis of exclusion [5-6].

Every patient with posterior ION who is older than 50 years old should be evaluated for giant-cell arteritis.

Arteritic ION

Diagnosis and Clinical Presentation: Although other vasculitides may occasionally induce ION, giant-cell arteritis is by far the most prevalent cause of arteritic anterior and posterior ION. The most typical ophthalmic symptom of giant-cell arteritis is anterior ION. Ophthalmic crises like arteritic anterior ION and arteritic posterior ION must be identified and treated quickly to avoid irreparable vision loss. The most feared side effect of giant-cell arteritis, which affects 20% of patients, is visual loss. Arteritic ION has a similar clinical appearance to nonarteritic ION, but there are a few "red flags" that might cause a clinical suspicion of arteritic ION [4].

Treatment

Identification and treatment of giant-cell arteritis are a serious medical emergency due to the disorder's curable nature and the catastrophic visual effects of a postponed diagnosis. The likelihood of visual loss caused by giantcell arteritis in the second eye increases in the hours to days after a patient loses vision in one eye. Giant-cell arteritis is particularly susceptible to glucocorticoids, and systemic symptoms including headaches, tenderness in the scalp, weariness, fever, and myalgias immediately go away. Glucocorticoids are given right away to stop vision loss in the unaffected eye, although they frequently do not restore vision that has already been lost.

Perioperative ION

Numerous non-ocular operations have the potential to cause both anterior and posterior ION, both of which frequently result in devastating bilateral vision loss. Although extended spinal fusion surgery with the patient prone and coronary artery bypass grafting are the two operations most frequently linked to ION, the documented prevalence of this complication even with both procedures is still less than 0.3 percent. The majority of occurrences of anterior ION are related to heart surgery, whereas posterior ION is more frequently confirmed in individuals who have had spine surgery. The origins of perioperative ION are not well understood, and the contributing elements in these two procedures are likely multiple and distinct [7].

Clinical examinations are the main component of ION diagnosis, and ION must be distinguished from other causes of ocular neuropathies.  Patients with ION who are older than 50 years old should be evaluated for giant-cell arteritis, and laboratory testing should be carried out with the appropriate level of suspicion. 

Despite the fact that there is no effective treatment for ION, the recent development of animal models is anticipated to spur the testing of novel therapeutic strategies [3,8].

1. " The Neurologist [Internet]. [cited 2022 Jul 25]. Available from: https://journals.lww.com/theneurologist/Abstract/2008 /11000/Ischemic_Optic_Neuropathies.2.aspx

2. Luneau K et al. "Ischemic optic neuropathies." Neurologist, vol. 14, no. 6, 2008, pp. 341–354. Available from: https://journals.lww.com/theneurologist/Fulltext/2008/11000/Ischemic_Optic_Neuropathies.2.aspx

3. Berry S. et al. "Nonarteritic anterior ischemic optic neuropathy cause effect and management." Eye Brain, vol. 9, 2017, pp. 23–28. Available from: https://www. dovepress.com/nonarteritic-anterior-ischemic-optic-neuropathy-cause-effect-and-manag-peer-reviewed-fulltext-article-EB

4. "Anterior ischemic optic neuropathy (AION) background pathophysiology epidemiology." Medscape [Internet]. [cited 2022 Jul 25]. Available from: https://emedicine.medsca pe.com/article/1216891-overview

5. Hayreh S.S. "Ischemic optic neuropathy." Prog. Retin. Eye Res., vol. 28, no. 1, 2009, pp. 34–62.

6. Atkins E.J. et al. "Treatment of nonarteritic anterior ischemic optic neuropathy." [Journal name not provided]

7. Hayreh S.S. "Management of ischemic optic neuropathies." Indian J. Ophthalmol., vol. 59, no. 2, 2011, pp. 123. Available from: /pmc/articles/PMC3116541/

8. Gibbons A and Henderson A.D. "Non-arteritic anterior ischemic optic neuropathy challenges for the future." Front. Ophthalmol., 2022, pp. 12.