Version May 2024
INTRODUCTION — Ischemic optic neuropathy is the most common acute optic nerve disorder in patients over age 50 years [1]. Ischemic optic neuropathy is generally categorized as anterior (affecting the optic disc) versus posterior (retrobulbar), and as arteritic versus nonarteritic. Anterior involvement is usual with both arteritic and nonarteritic ischemic optic neuropathy.
Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common form of ischemic optic neuropathy. It is an idiopathic, ischemic insult of the optic nerve head characterized by acute, monocular, painless visual loss with optic disc swelling.
This topic will discuss the prognosis and treatment of NAION. The epidemiology, pathogenesis, etiologies, clinical features, and diagnosis of NAION are discussed separately. Other forms of ischemic optic neuropathy and other optic neuropathies are discussed separately. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies" and "Nonarteritic anterior ischemic optic neuropathy: Clinical features and diagnosis" and "Clinical manifestations of giant cell arteritis" and "Optic neuropathies".)
PROGNOSIS
Clinical course and visual outcomes — After the onset of NAION, vision may continue to deteriorate in some patients over the first few days or weeks. In the Ischemic Optic Neuropathy Decompression Trial (IONDT), 207 patients with an initial visual acuity of 20/64 were reevaluated within 30 days; 29 percent of these patients had progressed [2]. Others report that among patients with a broad spectrum of visual loss at presentation, 5 to 11 percent of patients have significant visual acuity worsening over this time period [3,4].
After this initial period of potential visual decline, most patients stabilize. In the IONDT, objective visual improvement was noted in 43 percent of patients with vision worse than 20/60 at baseline. However, recovery of visual fields is less common, and most patients do not experience significant improvement in their vision [3,5-8].
No specific demographic factor or comorbidity (eg, age, sex, diabetes, hypertension) has been associated with visual outcome [4].
Disc edema typically resolves over two to three months and is followed by optic disc pallor [9]. At six months, the disc appears pale, usually in a diffuse, but sometimes sectoral, pattern [10]. In contrast to patients with giant cell arteritis, patients with NAION do not develop clinically evident optic nerve cupping [11,12].
Continued progression after the first few weeks is unusual; progressive worsening or persistence of disc swelling should prompt investigation into alternative causes of vision loss. (See "Nonarteritic anterior ischemic optic neuropathy: Clinical features and diagnosis", section on 'Diagnosis'.)
Recurrence
●Ipsilateral recurrence – Recurrence of NAION in the affected eye is not common; studies report a less than 6 percent same-eye recurrence rate at two years, which may increase to as high as 7.6 percent at three years [1,13,14].
●Contralateral events – The risk of NAION in the fellow eye was traditionally believed to be quite high, but prospective studies have found it to be lower than previously thought, with an estimated five-year cumulative incidence of 12 to 19 percent [15,16]. In the IONDT, 418 patients with NAION were prospectively evaluated [16]. At baseline, 21 percent had a history or clinical evidence of NAION in the fellow eye. After a median follow-up of five years, 15 percent of patients developed NAION in the other eye, with a median interval between events of 1.2 years (range 16 days to 6 years).
●Risk factors – Diabetes and worse baseline visual acuity in the affected eye have been identified as risk factors for recurrence, but older age, sex, hypertension, anemia, migraine, and smoking have not [16,17]. Patients with diabetes are also more likely to have second-eye involvement at baseline [18]. Younger patients may be at greater risk of recurrence. In a retrospective study of 164 patients less than 50 years in age, 5 percent had evidence of fellow-eye involvement at baseline, 5 percent had simultaneous bilateral involvement, and 32 percent had sequential involvement with a median time between events of 1 year (range 1 week to 14 years) [14].
In many series, the severity of the initial event appears to predict the severity of the subsequent event [1,2,16,19]; however, one-third of patients will have a greater than six-line difference in visual acuities between affected eyes, making an initial mild event not entirely reassuring [17,20].
Mortality and other vascular events — Whether NAION indicates a patient at increased risk for cardiac and cerebrovascular event is uncertain. Some studies have not found an increased risk following NAION [21-24]. However, others have reported an increased risk of stroke and myocardial infarction [25,26]. As examples:
●In a large prospective series of 406 patients, a higher cerebrovascular and cardiovascular risk after NAION was reported, although an adjustment for diabetes and hypertension as independent cerebrovascular risk factors was not made [26].
●A more recent study of 97 patients with NAION found a similar incidence of cerebrovascular and coronary ischemic events following NAION compared with risk factor- and age-matched controls in the Framingham and United Kingdom Prospective Diabetes Study database [24].
TREATMENT — There is no therapy proven to ameliorate the degree of visual impairment in NAION [1,27,28].
Novel therapies for NAION are being developed. While some studies suggest a potential vision benefit, none have been confirmed in randomized trials. Thus, such treatments are considered investigational. (See 'Other investigational treatments' below.)
Blood pressure management — Patients who develop NAION in the setting of severe systemic hypotension may benefit from prompt efforts to reverse hypotension, according to uncontrolled observations [29,30]. If this has occurred in the setting of acute blood loss, blood transfusion is advised.
Patients with acutely elevated blood pressure should have their blood pressure lowered incrementally rather than abruptly, as this has been described as precipitating NAION in at least one case report [29].
Acute medical treatments with uncertain or no benefit
Acute aspirin therapy — Aspirin therapy does not appear to influence visual outcomes of acute NAION. In a retrospective case-control study, 23 patients treated with aspirin before and during the course of NAION were compared with 55 patients with NAION who did not use aspirin [31]. Visual outcomes (visual acuity and mean deviation on automated perimetry) were similar in the two groups.
Studies investigating aspirin therapy in the secondary prevention of vascular outcomes are discussed separately. (See 'Secondary prevention' below.)
Glucocorticoids — Glucocorticoid therapy is not a recommended treatment in NAION as the evidence supporting its efficacy is limited. However, glucocorticoids are sometimes used in NAION when there is concern that giant cell arteritis has not been excluded and in cases of severe bilateral vision loss, as can occur in the perioperative or dialysis setting, despite the absence of compelling evidence [32,33]. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies", section on 'Perioperative ischemic optic neuropathy'.)
Studies evaluating a potential role of glucocorticoids are of low quality. While some anecdotal reports and nonrandomized studies suggest that glucocorticoids may have some benefit in NAION [34-37], other observational studies have not found that glucocorticoid treatment is efficacious [38,39]. In a meta-analysis of eight mostly nonrandomized studies (720 eyes), glucocorticoid therapy was not associated with a benefit on visual acuity outcomes [40]. Two small randomized trials (38 and 90 patients) did not find a benefit for glucocorticoids on visual outcomes [41,42].
Studies investigating intravitreal glucocorticoid therapy are discussed separately. (See 'Other investigational treatments' below.)
Surgical therapies with uncertain or no benefit
Optic nerve sheath decompression — In optic nerve sheath decompression surgery (ONDS), two or more slits or a window in the optic nerve sheath are created. This procedure allows cerebrospinal fluid to escape, purportedly reducing the pressure surrounding the optic nerve. Compression of the optic nerve sheath is possibly pathogenic in NAION, and in initial reports, this appeared to be a promising strategy in reducing optic nerve damage in NAION [43].
The effectiveness of ONDS was evaluated in the Ischemic Optic Neuropathy Decompression Trial (IONDT) [2]. The trial was stopped early. The initial report of the IONDT described six-month outcomes in 244 patients with NAION with age >50 years and a baseline visual acuity worse than 20/64 [8]. Improved visual acuity by at least three lines occurred in 33 percent of the surgical group compared with 43 percent of controls. Visual acuity worsened by at least three lines in 24 percent of the surgical group compared with 12 percent of controls. These results indicate no benefit and possible harm from surgery. In a follow-up report, outcomes at 24 months were similar in treatment groups; vision improved in 31 percent of the surgery group and in 29 percent of controls, while 20 percent in the surgery and 22 percent in the control group had worsened visual acuity compared with baseline [7]. Adverse effects of surgery included pain, diplopia, and central retinal artery occlusion.
The conclusions of IONDT were that ONDS appears to be of no value to most patients with NAION and could potentially cause further visual deterioration [2,44]. An unexpectedly high rate of spontaneous improvement in visual acuity was observed in controls [2,8]. ONDS was associated with a lower rate of improvement; at 3, 6, and 12 months of follow-up, patients receiving surgery had a greater risk of losing three or more lines of vision.
Optic neurotomy — This investigational surgical procedure relaxes the scleral ring surrounding the prelaminar and laminar regions of the optic nerve head, with the goal of reducing constriction and preventing necrosis of underperfused nerve fibers. In one study, seven selected patients with severe vision loss (<20/800) from NAION underwent transvitreal nasal radial optic neurotomy [45]. Six patients had visual improvement. The mean preoperative visual acuity was 20/2400. After a mean 13 weeks following surgery, the mean visual acuity was 20/250, with an average of 10 lines of improvement. In the two patients with sufficient visual acuity for preoperative perimetry, visual fields also significantly improved after surgery.
While this report appears somewhat promising, there was no control group for comparison and only a few patients were included. Others are skeptical regarding the potential biomechanical effect of this procedure [46]. Moreover, while serious complications were not reported in this series, surgical manipulation of the optic nerve head has the potential to further damage nerve fibers and blood vessels, potentially causing devastating loss of vision [47].
Vitrectomy — In one case series, 16 patients with NAION had findings on optical coherence tomography and ultrasound that were consistent with partial posterior vitreous detachment [48]. The authors postulated that elevation of the optic nerve head from traction of the posterior vitreous may have disrupted the microcirculation and axoplasmic flow, leading to optic nerve edema and visual dysfunction. Surgical release of epipapillary vitreous traction via vitrectomy was performed within one month, with visual acuity improvement noted in 15 patients, 9 of whom had greater than three lines of improvement.
This was an uncontrolled case series. The findings need to be independently confirmed before this treatment should be adopted. Other authors have disputed the findings and conclusions of this report [49-51]. However, this study raises the possibility of a role of vitreous traction in the pathogenesis of NAION.
Other investigational treatments — Research efforts continue to focus on development of a treatment for NAION. Neuroprotective medications that will help with preventing retinal ganglion cell and axonal loss have been tried in animal models. Neuroprotective and neuroregenerative treatments are being investigated both for acute management and for late-stage recovery.
●Citicoline – Citicoline is a putative neuroprotective agent that has been evaluated in the treatment of acute cerebral infarction. Preliminary studies in NAION suggest that it may provide modest benefit.
In a randomized pilot study, 14 patients with NAION were treated with citicoline 1600 mg per day for 60 days. After 60 and 180 days, these treated patients demonstrated overall improvement in visual acuity compared with baseline, while untreated patients did not [52]. Another randomized study evaluated the efficacy of citicoline prescribed daily for six months in 36 patients who were diagnosed with NAION in the preceding 6 to 12 months [53]. At six- and nine-month evaluations, improvement in visual acuity was noted in treated patients versus nontreated patients.
●Levodopa – A potential role for dopamine in the treatment of NAION is based on its putative neuroprotective and neuromodulatory effects in the retina, optic nerve, and/or brain, or its activity as a neurotransmitter in the retina.
In a nonrandomized study, 18 patients with acute NAION were treated with a three-week course of levodopa within 45 days of vision loss [54]. Outcomes were compared with 19 untreated controls. At six months, levodopa-treated patients were more likely to have had three lines or greater improvement in visual acuity than controls (77 versus 20 percent). No improvement in visual fields was noted. The statistical analysis and handling of confounding variables in this study have been criticized [55].
Levodopa has also been studied for its potential to aid visual recovery in patients with chronic NAION. An unblinded but randomized study in 20 patients with NAION of at least six months duration found that a six-week course of levodopa treatment was associated with significant improvement in visual acuity but had no effect on field loss or color vision [56]. A similar study, performed in 24 patients with a mean duration of NAION of more than 10 months, found no benefit for levodopa on visual outcomes [57].
●Brimonidine – Brimonidine is an alpha-2 agonist that lowers intraocular pressure and is used in the treatment of glaucoma. There have been promising reports from animal studies suggesting that topical brimonidine may have a neuroprotective effect on retinal ganglion cells and reduce optic nerve injury after ischemia [58-60]. However, a randomized placebo-controlled trial found no therapeutic effect of brimonidine 0.2 percent in 36 patients with acute NAION [61]. Moreover, an open-label study of 14 patients treated with brimonidine suggested a trend for worse visual acuity and fields in treated patients compared with matched controls [62].
●Systemic erythropoietin – Erythropoietin has potential neuroprotective effects after ischemic injury. In a prospective nonrandomized study of 113 consecutive patients with acute NAION, patients received either systemic intravenous glucocorticoid combined with recombinant human erythropoietin, systemic corticosteroid alone, or neither [63]. Vision outcomes were similar in all patient groups.
●Intravitreal agents – Intravitreal administration of medications offers the promise of delivering targeted medications directly to the source of pathology. However, this route of administration is not without risks, including a small risk of infectious endophthalmitis, retinal detachment, and traumatic cataract estimated at approximately 0.15 percent [64]. None of the agents discussed below are currently recommended in the treatment of NAION.
•Triamcinolone – Intravitreal triamcinolone acetonide (IVTA), a glucocorticoid, has been administered to patients with NAION with suggested benefit in small case series [65-67]. In one case, treatment was complicated by increase in intraocular pressure requiring antiglaucoma treatment, a complication that occurs in up to 25 percent of patients when IVTA is administered for other indications [68,69].
A retrospective study compared outcomes in 21 patients with NAION who were given a single intravitreal injection of 4 mg of triamcinolone and 15 nontreated patients; both visual acuity and visual fields were improved at six months in the treated versus the nontreated group [70]. In addition, delay to injection was inversely associated with visual acuity achieved at six months.
Further study in a large randomized trial is needed to confirm the benefits of this treatment.
•Anti-vascular endothelial growth factor (VEGF) agents – VEGF is a signaling protein that stimulates angiogenesis and increases microvascular permeability. Anti-VEGF agents such as bevacizumab and ranibizumab have the potential to reduce vasogenic edema and may play a role in decreasing optic nerve head edema and secondary tissue injury.
While at least two case reports describe rapid resolution of vision loss and disc edema in patients with NAION treated with intravitreal ranibizumab and bevacizumab [71,72], a small nonrandomized study found that visual outcomes were similar in the 17 patients treated with intravitreal bevacizumab compared with eight patients who were not so treated [73].
•Erythropoietin – Erythropoietin has potential neuroprotective and possibly neuroregenerative effects after ischemic injury. In one case series, 31 patients with NAION received unilateral intravitreal erythropoietin injection (2000 units) within one month of onset of NAION [74]. Visual acuity improvement occurred in 61 percent of patients within the first month. Vision continued to improve up to three months and then deteriorated, but remained significantly better than baseline at the last six-month follow-up examination.
Another study in 16 patients with late-stage optic neuropathy and found no benefit from intravitreal erythropoietin injection [75].
•Granulocyte colony-stimulating factor (G-CSF) – G-CSF is a neuroprotective agent evaluated in a prospective interventional case series where 14 eyes of 14 patients with NAION received intravitreal injection of G-CSF within two weeks of the onset [76]. The best-corrected visual acuity improved in the first month following injections but decreased subsequently; the final visual acuity was similar to baseline measurements. Visual field parameters were also not improved. While the drug was found to be safe, the beneficial effect only lasted a month.
•QPI-1007 – QPI-1007 is a chemically modified small interfering RNA targeting the expression of the caspase 2 protein, which accumulates in ischemically injured cells and may contribute to apoptosis [77]. QPI-1007 has been studied in NAION, including in a randomized trial of more than 700 patients with acute NAION. Study results have not yet been published [78].
●Fibrinogen/low-density lipoprotein (LDL) apheresis – Fibrinogen/LDL apheresis, also known as heparin-induced extracorporeal LDL/fibrinogen precipitation (HELP), removes fibrinogen, total cholesterol, LDLs, and triglycerides from plasma and has shown promise in the treatment of microvascular disorders, including peripheral artery disease and sudden hearing loss [79,80].
In a small, randomized study of 40 patients with recent-onset NAION, visual outcomes were similar in patients assigned to treatment with HELP and those assigned to hemodilution therapy [81].
●Hyperbaric oxygen – While case reports have suggested a possible benefit for hyperbaric oxygen in the treatment of NAION, these findings have not been confirmed in well-designed studies [82]. A nonrandomized study compared hyperbaric oxygen treatment in 20 patients with acute NAION with 27 untreated patients and found no significant difference in visual acuity or visual field outcomes in the groups [83].
●Stem cell therapy – Stem cell therapy has been reported to improve vision in patients with chronic NAION in uncontrolled case series. Possible mechanisms by which visual improvement may occur include paracrine secretion of proteins and hormones, transfer of mitochondria, release of messenger RNA or other compounds via exosomes or microvesicles, and neuronal transdifferentiation of the stem cells [84].
Ten patients with bilateral visual loss due to sequential NAION underwent autologous bone marrow-derived stem cell (BMSC) therapy within the Stem Cell Ophthalmology Treatment Study (SCOTS) [84]. Average duration of visual loss was 9.8 years, and affected eyes were treated with either retrobulbar, subtenon, and intravenous BMSC therapy or, following vitrectomy, intraoptic nerve, subtenon, and intravenous BMSC therapy. Immediately following therapy, 80 percent of patients experienced improvement in Snellen binocular vision and 20 percent remained stable; in follow-up, 74 percent of eyes treated gained vision and 16 percent remained stable. The authors concluded that meaningful visual improvements were seen in a significant percentage of the patients with NAION.
●RPh201 – RPh201 is a botanical extract of gum mastic or "Arabic gum" that is believed to have neuroprotective effects [77].
A preliminary randomized trial evaluated 20 patients with NAION diagnosed six months to three years earlier. After 26 weeks of treatment, visual acuity improved by ≥15 letters in 36 percent of eyes in the active treatment group compared with 12 percent of those who received placebo [85]. Overall, 64 percent of treated patients showed improvement in visual acuity compared with 38 percent in placebo-treated patients. A larger follow-up trial is underway [86].
SECONDARY PREVENTION — There is no known effective therapy proven to prevent NAION in the fellow eye [1,27]. Most patients with NAION are treated with daily aspirin and risk factor management.
Aspirin — We make recommendations for long-term aspirin therapy based upon the individual patient's other risk factors and comorbidities rather than on an episode of NAION, as it is unclear that aspirin is beneficial in regard to prevention of NAION recurrence.
Four retrospective studies have evaluated the role of aspirin in the prevention of NAION in the fellow eye with somewhat mixed results. One case-control and one retrospective study, each involving only a few patients, suggested that aspirin therapy was associated with a reduced risk of fellow-eye involvement [17,87]. However, larger retrospective studies have not found evidence of benefit [15,16]. The largest study compared outcomes in 153 patients who had received aspirin following the development of unilateral NAION and 278 who had not [15]. After five years, the cumulative probability of NAION in the fellow eye was similar in the aspirin and no-aspirin groups (17 and 20 percent, respectively).
Although there isn't sufficient evidence to support aspirin therapy as secondary prevention in NAION, many patients with NAION will be appropriately treated with aspirin therapy on the basis of comorbid vascular disease and/or their underlying vasculopathic risk factors that independently place them at risk for cardiovascular disease and stroke. (See "Overview of primary prevention of cardiovascular disease".)
Associated conditions and medications
●Hypercoagulable conditions – Patients found to have an underlying hypercoagulable condition may benefit from anticoagulation, as such treatment may prevent future thromboembolic events [88]. See individual topic reviews regarding specific conditions.
●Phosphodiesterase 5 (PDE-5) inhibitors – While the association between NAION and PDE-5 inhibitors is unproven, patients who have suffered an event of NAION should be counseled about potential ocular side effects [89,90]. The US Food and Drug Administration (FDA) has advised patients "to stop use of all PDE-5 inhibitors…and seek medical attention in the event of sudden loss of vision in one or both eyes," and that these medications "should be used with caution, and only when the anticipated benefits outweigh the risks, in patients with a history of NAION" [91].
The data describing the possible association between NAION and PDE-5 inhibitors are discussed separately. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies", section on 'Phosphodiesterase-5 inhibitors'.)
●Other implicated medications – Patients with NAION who are taking other implicated medications (eg, amiodarone, interferon alpha, sympathomimetics) should be counseled about the possible association, and alternatives should be considered if available.
The data describing the possible association between NAION and these medications are discussed separately. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies", section on 'Medications'.)
●Sleep apnea – Patients with sleep apnea are likely to benefit from treatment, although in one case series of three patients, treatment of sleep apnea did not appear to prevent NAION [92]. In patients with suspicious history for sleep apnea, formal testing should be recommended and treatment offered when indicated. The possible association between sleep apnea and NAION is described separately. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies", section on 'Sleep apnea syndrome'.)
Vascular risk factor management — Medical control of underlying vasculopathic risk factors (eg, hypertension, diabetes, and smoking) is indicated in the primary prevention of cardiovascular disease and stroke; it is not known whether such interventions decrease the risk of NAION recurrence.
Patients with acutely elevated blood pressure should have their blood pressure lowered incrementally rather than abruptly, as this has been described as precipitating NAION in at least one case report [29]. Over-aggressive control of systemic arterial hypertension may produce nocturnal hypotension, which is believed to be a risk factor for NAION [93]. Patients should be counseled against taking bedtime antihypertensive agents to minimize the risk of nocturnal hypotension. Morning administration of blood pressure medications should be considered. (See "Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies", section on 'Nocturnal hypotension'.)
VISUAL REHABILITATION — More than 50 percent of patients with NAION are left with visual acuity less than 20/200 with constricted visual fields. These patients may benefit from visual rehabilitation offered by low-vision services [94,95].
We do not recommend to our patients a new modality called vision restoration therapy (VRT), which uses a computer program to stimulate areas of residual vision in patients with visual field defects, and which has been advocated for patients with low vision. A randomized, double-blind pilot trial to evaluate the effects of VRT on the visual function in 10 patients with NAION found a nonsignificant trend toward benefit of visual function [96]. However, VRT remains controversial and unproven, and so far there is very little evidence to support the use of VRT as part of low-vision interventions offered to patients with optic neuropathies.
SUMMARY AND RECOMMENDATIONS
●Clinical course – Patients with acute nonarteritic anterior ischemic optic neuropathy (NAION) have a 5 to 10 percent incidence of significant visual acuity worsening over the first several days to few weeks. In most patients, vision then subsequently stabilizes and rarely improves. (See 'Clinical course and visual outcomes' above.)
●Risk of recurrence in same or fellow eye – Over a period of five years after NAION, patients have a 5 to 7 percent risk of recurrence in the same eye, and a 15 to 19 percent risk of recurrence in the fellow eye. Diabetes and greater severity of NAION in the initially affected eye are risk factors for fellow-eye NAION. (See 'Recurrence' above.)
●Cardiovascular prognosis – Patients with NAION do not appear to have a higher mortality or risk for stroke or cardiovascular disease than would otherwise be expected on the basis of their underlying comorbidities. (See 'Mortality and other vascular events' above.)
●Acute management – No treatment for NAION has been shown to improve visual acuity outcomes or reduce the risk of recurrence. (See 'Treatment' above.)
Patients with acutely elevated blood pressure should have their blood pressure lowered incrementally rather than abruptly to avoid the theoretical risk of exacerbating vision loss. (See 'Blood pressure management' above.)
Optic nerve sheath decompression surgery (ONDS) is not beneficial and is even potentially harmful to vision. (See 'Optic nerve sheath decompression' above.)
●Secondary prevention – While aspirin and vascular risk factor management have not been shown to improve visual outcomes or reduce recurrence in patients with NAION, these interventions are appropriate for most patients to reduce their risk of stroke and cardiovascular events based on their comorbid risk factors and vascular disease. (See "Overview of primary prevention of cardiovascular disease".)
We generally advise morning administration of blood pressure medications to avoid nocturnal hypotension, which may be a risk factor for recurrence of NAION. (See 'Vascular risk factor management' above.)
In patients with unilateral NAION, we suggest discontinuation of implicated medications (phosphodiesterase 5 [PDE-5] inhibitors, amiodarone, interferon alpha, sympathomimetics) when possible (Grade 2C), given the potential for increasing the risk of second-eye involvement. (See 'Associated conditions and medications' above.)
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