ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies

Nonarteritic anterior ischemic optic neuropathy: Epidemiology, pathogenesis, and etiologies
Literature review current through: May 2024.
This topic last updated: May 09, 2024.

INTRODUCTION — Ischemic optic neuropathy is the most common 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 [2]. 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 epidemiology, pathogenesis, and causes of NAION. The clinical features, diagnosis, treatment, and prognosis of NAION are discussed separately. Other forms of ischemic optic neuropathy and other optic neuropathies are discussed separately. (See "Nonarteritic anterior ischemic optic neuropathy: Clinical features and diagnosis" and "Nonarteritic anterior ischemic optic neuropathy: Prognosis and treatment" and "Clinical manifestations of giant cell arteritis" and "Optic neuropathies".)

VASCULAR ANATOMY — The optic nerve head (prelaminar and laminar portions) is supplied by 15 to 20 short posterior ciliary arteries that are derived from the ophthalmic artery and also by arterial branches from the anastomotic circle of Zinn-Haller [3-5]. The circle of Zinn-Haller itself is fed by the short posterior ciliary arteries, branches of pial arterial network, and choroidal vessels (figure 1).

This vascular supply may demonstrate distinct upper and lower halves consistent with altitudinal damage to the optic nerve head [6]. (See "Nonarteritic anterior ischemic optic neuropathy: Clinical features and diagnosis".)

The retina is supplied by the choroidal circulation and branches of the central retinal artery, both derived from the ophthalmic artery, a branch of the internal carotid artery. (See "Central and branch retinal artery occlusion", section on 'Vascular anatomy'.)

EPIDEMIOLOGY — NAION is the most common optic neuropathy in middle aged and older adult patients, and constitutes 94 percent of all anterior ischemic optic neuropathy cases [7]. The estimated annual incidence in the United States is 0.54 per 100,000 for all ages and 2.3 to 10.2 per every 100,000 persons older than 50 years, with similar rates in other countries [8-11]. There are approximately 6000 new cases annually.

NAION primarily occurs in older adults. The Ischemic Optic Neuropathy Decompression Trial (IONDT), a large prospective study population with age-defined entry criteria, reported a mean age of 66 years [8]. Other population-based studies report a mean age of 61 to 72 years [10,12]. NAION is considered unusual in patients under 45 years of age. However, in one case series of patients evaluated at a subspecialty clinic, 23 percent of individuals were less than 50 years old [13].

White individuals appear to be at higher risk than other ethnic groups [8,9]. NAION affects males and females equally [8,9,14].

PATHOGENESIS — NAION is believed to result from acute ischemia to the optic nerve head [2]. However, the precise mechanism leading to optic disc ischemia is unclear. There has been histopathologic documentation of infarction, but not vasculopathy in NAION [6,15,16]. Because retinal or cerebral emboli are rarely detected in the setting of NAION, embolism from cardiac or larger artery disease is believed to underlie few, if any, NAION [1,6]. In contrast to retinal ischemia, NAION is not associated with carotid occlusive disease [17,18].

Because of its strong association with age, diabetes, hypertension, and the known vascular supply of the optic nerve head, small arterial occlusive disease has been proposed as a mechanism of NAION. A magnetic resonance imaging study of 13 patients with NAION demonstrated a higher burden of white matter ischemic lesions compared with controls matched for age, hypertension, and diabetes [19]. However, a small artery vasculopathy affecting the optic nerve circulation has not been pathologically identified in NAION patients.

One hypothesis is that NAION results from transient hypoperfusion of the posterior ciliary arteries [6]. Fluorescein angiography in acute NAION shows delayed arterial filling, a finding that is not observed in cases of optic disc edema due to other etiologies [20,21]. Blood flow to the optic nerve head is maintained by autoregulatory mechanisms that include autonomic input to the blood vessels and release of vasoactive substances such as endothelin (vasoconstrictor) and nitric oxide (vasodilator). Disturbance in autoregulatory mechanisms may be induced by arteriosclerosis, vasospasm, and antihypertensive medications. In this setting, a critical fall of perfusion pressure in the capillaries supplying the optic nerve head may be caused either by a marked fall in blood pressure, a rise in the eye pressure, or blockage or sudden, severe narrowing of the internal carotid artery and/or ophthalmic artery (see 'Etiology and risk factors' below). Vasospasm has also been speculated to play a role [6,22,23].

Another theory is that NAION results from a process similar to that of a compartment syndrome. Some argue that the histopathologic characteristics of the injury, which, in some cases, included cavernous degeneration with substantial compression of adjacent normal axons by the degenerated nerve tissue, most favor this pathogenic mechanism [15,16]. Patients with NAION are believed to have a premorbid abnormality of optic disc structure (ie, a small cup with crowded optic nerve fibers) that predisposes them to NAION (see 'Ocular risk factors' below). The effects of structural crowding in the optic nerve head may lead to mechanical obstruction of axoplasmic flow causing axonal swelling and/or secondary compression of the microcirculation due to axoplasmic stasis [6]. The fact that a recurrence of NAION is uncommon in the same eye may support this hypothesis, as the atrophy that follows ischemic injury may relieve nerve fiber crowding [1].

Others have proposed that occlusion of tributaries of the central retinal vein is the initial event in NAION, which leads to optic nerve head edema and secondary arteriolar constriction causing an ischemic infarction of the optic nerve [24]. Purported risk factors such as sleep apnea and recumbent posture may cause an increase in venous pressure. Vasodilation of the central retinal artery causing a secondary obstruction of central retinal vein or its tributaries may also explain NAION occurring in association with prolonged hypotension, nocturnal hypotension, and use of phosphodiesterase-5 (PDE-5) inhibitors.

The most commonly proposed pathogenetic theory combines these mechanisms, proposing that insufficiency of the optic disc circulation causes ischemia and swelling of the optic nerve, which in the setting of a crowded optic nerve head leads to infarction.

ETIOLOGY AND RISK FACTORS — Most cases of NAION occur apparently spontaneously in the setting of one or more underlying atherosclerosis risk factors. In many case series and some case-control studies, several risk factors for NAION have been identified or suggested (table 1).

Atherosclerosis — Consistent with its presumed ischemic pathogenesis, atherosclerotic risk factors, smoking, hypertension, and diabetes have been associated with an increased risk of NAION; in the Ischemic Optic Neuropathy Decompression Trial (IONDT), one of these was present in 60 percent of patients [8]. Overall, systemic hypertension has been reported in 34 to 49 percent of patients, while diabetes is seen in 5 to 28 percent of patients [8,12,13,25-27]. NAION patients younger than 50 years old have a stronger association with diabetes, hypertension, and hypercholesterolemia than older patients [28-30].

Ischemic heart disease, hypercholesterolemia, stroke, tobacco use, and atherosclerosis have also been associated with NAION, but more variably [12,25-27,29-33].

Nocturnal hypotension — Twenty-four hour ambulatory blood pressure recordings demonstrate a physiologic drop in systemic blood pressure during sleep that normalizes on awakening in the morning. Some evidence suggests that this nocturnal arterial hypotension may play a role in the development of NAION [34-36]. Patients with NAION often discover vision loss upon awakening [37]. Patients with systemic hypertension and secondary impairment of autoregulation of the optic circulation may be particularly vulnerable to this putative complication of nocturnal hypotension [28,36].

Nocturnal blood pressure decreases may be exacerbated by antihypertensive medications, particularly when administered at night [38]. Implicated medications include beta-blockers (oral agents and eyedrops), calcium-channel blockers, angiotensin converting enzyme inhibitors, terazosin hydrochloride, amitriptyline, and other similar compounds [28,36,38,39]. However, marked nocturnal hypotension has also been recorded in patients not taking such medications.

One investigation found that patients with NAION had greater depressions in nocturnal blood pressure compared with controls, but this was not confirmed in another independent case series [28,40].

Prothrombotic risk factors — A number of case reports have described NAION occurring in individuals with coagulation abnormalities [41-46]. However, systematic studies have not defined a clear association for all coagulation abnormalities. As an example, elevated homocysteine levels have been found in some case series of patients with NAION [47-49], but not in others [50].

One small case-control study of 25 patients with NAION found increased odds of activated protein C resistance and factor V Leiden mutation (odds ratio [OR] 4.97, 95% CI 1.3-19.5) [51]. However, another case-control study of 61 patients with NAION did not find an association between the prothrombotic risk factors lupus anticoagulant, protein C or protein S, and antithrombin III, or prothrombotic polymorphisms in the genes for factor V, II, or methylenetetrahydrofolate reductase [27]. In a follow-up investigation in this population, a significant association between a platelet polymorphism involving the glycoprotein Ib-alpha gene and NAION was identified [52]. Patients carrying this allele were also more likely to have subsequent second eye involvement. It is speculated that this genetic change makes platelets more vulnerable to activation.

The results of a comprehensive battery of coagulation studies were compared in a group of 35 patients with NAION who were younger than 65 years and 70 age- and sex-matched healthy controls [53]. An abnormality was found in 51 percent of patients and 17 percent of controls. The most frequent abnormalities were an increased level of factor VIII and lipoprotein a. A family history of thromboembolism, age ≤55 years, and absence of cardiovascular risk factors were predictors of a coagulation abnormality.

Ocular risk factors — It is believed that an important risk factor for NAION is a small optic nerve head with a small or absent physiologic cup. In one case series, this finding was noted in 82 percent of patients [13]. Case-control studies have found a significantly smaller cup-to-disc ratio in the unaffected eye in patients with NAION [27,54-58]. Optic disc drusen is another disc anomaly that is believed to be associated with nerve fiber crowding and may predispose to NAION [13,59]. By contrast, the unaffected optic nerve head is normal-appearing in patients with arteritic anterior ischemic optic neuropathy [60].

The association between NAION and cataract surgery has been debated [61,62]. A number of cases of NAION occurring in the first hours to weeks after surgery have been reported [63,64]. One case series found that if NAION occurs after one cataract surgery, the risk in the other eye is as high as 30 to 50 percent after a subsequent surgery [65]. NAION has also been a reported complication following LASIK procedures [66,67]. It is suggested that a perioperative rise in intraocular pressure leads to decreased perfusion of the optic nerve head, but this is unproven.

NAION is infrequently associated with other ocular conditions including acute angle closure glaucoma [68], prolonged pressure on the eyeball from any cause, and marked optic disc edema.

Sleep apnea syndrome — An association has been proposed between NAION and obstructive sleep apnea syndrome (SAS). One case control study found evidence of SAS on polysomnography in 71 percent of 17 patients with NAION versus 18 percent of 17 control patients referred for evaluation of possible restless legs syndrome [69]. Another case series found that 89 percent of 27 consecutively diagnosed NAION patients had SAS on polysomnography, a prevalence almost five times higher than expected based on other community-based studies [70,71]. A screening questionnaire for SAS was employed in another case control study of 73 NAION patients [72]. Cases were somewhat more likely than controls to report symptoms and characteristics consistent with SAS (OR 2.62, 95% CI 1.03-6.6).

SAS may increase the risk of NAION by several potential mechanisms: impaired optic nerve head blood flow autoregulation secondary to repeated apnea, optic nerve vascular dysregulation secondary to SAS-induced arterial blood flow variations, and direct optic nerve damage due to prolonged hypoxia [69,73]. One case series report of three patients with NAION and SAS suggests that treatment of SAS may not prevent NAION [74]. SAS may also be associated with increased intracranial hypertension and the pseudotumor cerebri syndrome. (See "Idiopathic intracranial hypertension (pseudotumor cerebri): Epidemiology and pathogenesis", section on 'Pathogenesis'.)

Renal failure — NAION has been reported in patients with renal failure on peritoneal or hemodialysis [75-81]. In contrast to other cases of NAION, children as young as 17 months are at risk [82-84]. A bilateral, but not necessarily symmetric, presentation is common.

Renal failure may contribute to the development of NAION via a number of mechanisms. The accelerated arteriosclerosis that occurs in patients with chronic renal failure may predispose patients to this complication. Most patients with NAION in this setting have either chronic hypotension or hypotensive episodes, usually related to dialysis. Anemia also appears to be a risk factor for NAION patients with renal failure [78]. Some speculate that a rise in intraocular pressure during hemodialysis may contribute to NAION; however, the effects of dialysis on intraocular pressure are disputed [84,85].

Volume replacement, along with restoration of blood pressure during hemodialysis, is reported to improve visual function in some patients [76,78,86].

Uremia is also speculated to produce a toxic optic neuropathy, characterized by a more slowly progressive vision loss, with decreased pupillary response and papilledema and improvement with dialysis [86,87].

Perioperative ischemic optic neuropathy — Perioperative ischemic optic neuropathy is a rare but potentially devastating complication of surgery and is the leading cause of postoperative blindness. (Other causes include retinal and cerebral ischemia [88-91].) In contrast to ischemic optic neuropathy occurring in other clinical settings, posterior rather than anterior ischemic optic neuropathy may be a more common postoperative complication, particularly in association with lumbar spine surgery and radical neck dissection [88]. (See "Posterior ischemic optic neuropathy", section on 'Perioperative PION'.)

Cardiopulmonary bypass (CABG) and spine surgeries are the procedures most often associated with NAION, but it has also been reported with many other surgeries, particularly bilateral radical neck dissection [92-96] and other chest, abdominal, neck, and orthopedic surgeries [97-100]. The incidence of ischemic optic neuropathy after CABG is reported between 0.06 and 0.5 percent [91,101-104] and after spine surgery is between 0.03 to 0.11 percent [4,90,91,105]. With other surgeries, it is a much less frequent complication, estimated at 0.0008 percent at one institution [106]. NAION may also occur after cataract and other eye surgeries. (See 'Ocular risk factors' above.)

Perioperative NAION usually presents with vision loss in the immediate postoperative period, after recovery from general anesthesia. Compared with other causes of NAION, the visual deficit is usually profound and often (in 53 to 66 percent) bilateral [88,91,102,107]. Because the erythrocyte sedimentation rate (ESR) and C-reactive protein can be elevated postoperatively in normal patients, these tests are not reliable in this setting to distinguish between arteritic ischemic optic neuropathy and NAION [108,109]. However, in the absence of presurgical symptoms that suggest giant cell arteritis, arteritic ischemic optic neuropathy in the postoperative setting is considered unlikely.

Risk factors for perioperative ischemic optic neuropathy include [88,89,91,92,97,99,101-105,107,108,110]:

Severe prolonged arterial hypotension

Hemodilution

Use of vasoconstricting agents, pressor support

Elevated pressor support

Anemia

Substantial blood loss, transfusion requirement

Longer operation time

Atherosclerotic risk factors

Small optic cup, optic nerve crowding

Use of the head-down or prone position used in some spinal surgeries may also increase orbital venous pressure by increasing intra-abdominal and intra-thoracic pressure, and is suggested to be a risk factor for ischemic optic neuropathy in these patients [88-90,105,111,112]. Alternatively, direct ocular compression from the headrest can occur in prone position and has been implicated as a cause of optic nerve head ischemia [89,112,113]. Risk factors for ischemic optic neuropathy more specific to spine surgery are discussed in detail separately. (See "Posterior ischemic optic neuropathy" and "Posterior ischemic optic neuropathy", section on 'Perioperative PION'.)

In patients undergoing radical neck dissection, increased orbital venous pressure may result from internal jugular vein ligation and lead to decreased arterial perfusion pressure at the optic nerve head [92,93,114]. Avoidance of simultaneous internal jugular vein ligation has been suggested to prevent this complication after radical neck dissection; however, staging the neck dissection does not appear to afford protection [92,94].

Efforts to rapidly correct hemodynamic derangements are recommended and may mitigate the severity of permanent vision loss, but there are no controlled observations to corroborate this as a treatment [89,90]. Similarly, avoidance of perioperative anemia with early transfusion has been suggested to prevent perioperative NAION, but a critical threshold of anemia or hypotension has not been identified [89,105,107].

Medications

Phosphodiesterase-5 inhibitors — The phosphodiesterase-5 (PDE-5) inhibitors sildenafil, vardenafil, and tadalafil are generally prescribed to treat male sexual dysfunction. Several reports link these drugs with NAION [115-122]. One study estimated an OR for the increased risk associated with PDE-5 inhibitors to be 2.4 (95% CI 1.3-4.2) [121]. It is not possible for observational studies to prove causation, and patients with sexual dysfunction often have vascular risk factors that are also associated with NAION [115,123,124]. In one case-control study, PDE-5 inhibitor prescription was not associated with NAION after controlling for diabetes, hypertension, and vascular disease [125]. As an exception, one case report describes NAION occurring in a child prescribed sildenafil for pulmonary hypertension [126].

While the relationship between these medications and NAION is unproven, the US Food and Drug Administration (FDA) has issued a warning regarding a possible association with NAION [127]. We suggest that patients with risk factors for NAION (eg, cardiovascular risk factors, sleep apnea, on antihypertensive drugs, history of prior NAION) be counseled against the use of these medications.

A causal relationship is suggested by the close temporal proximity of drug administration and symptom onset in many of these cases [121]. One case report in particular is compelling in describing multiple episodes of transient visual field loss, each episode occurring after taking tadalafil [128]. After a fifth dose, the patient experienced persistent monocular vision loss with clinical findings consistent with NAION. Two other cases have been described in which sequential symptoms were associated with drug rechallenge [115,129]. Another study examined visual fields in five healthy volunteers after taking sildenafil; one patient developed bilateral superior and inferonasal visual field depression [130]. At least two case reports document bilateral simultaneous NAION in patients taking PDE-5 inhibitors [118,120].

The mechanism by which PDE-5 inhibitors might cause NAION is not known. Some studies, although not others, suggest that in normal adults, these agents cause retinal vasodilation and increased optic nerve perfusion [131-134]. It is possible that in patients with microvascular disease and impaired autoregulation, these agents might cause a "shunting" of blood flow away from these vessels and induce ischemia [123]. In one case-control study, PDE-5 inhibitors were a risk factor for NAION only in the setting of comorbid cardiovascular disease or hypertension [135]. Another possible mechanism by which these drugs might be associated with NAION is their hypotensive effect, which, when they are used in the evening hours, could exacerbate nocturnal hypotension [123]. (See 'Nocturnal hypotension' above.)

A phase IV observational case-crossover study to assess whether PDE-5 inhibitors trigger NAION is ongoing [136]. The results of this study will provide useful data on the safety of these compounds and of patients at risk who should avoid their use.

Interferon-alpha — Interferon-alpha is used in the treatment of chronic hepatitis, as well as certain malignancies. NAION has been reported as an uncommon complication of interferon-alpha treatment [137-143]. NAION in these case reports tends to be bilateral and sequential, and may recur after restarting the medication. Clinical course is variable, with some patients improving after discontinuation of therapy. Possible pathogenic mechanisms include interferon-induced systemic hypotension, an immune complex deposition within the optic disc circulation, or another cytokine-mediated inflammatory reaction of the blood vessels.

Amiodarone — An association between amiodarone and NAION is uncertain [144]. Amiodarone has also been suggested to cause a toxic optic neuropathy, although this remains unproven as well. An optic neuropathy related to direct toxic effects of the drug is suspected in patients who have a more insidious onset of vision loss with slow progression and simultaneous bilateral involvement, features that are atypical of NAION [144-146]. (See "Optic neuropathies", section on 'Drugs and toxins' and "Amiodarone: Adverse effects, potential toxicities, and approach to monitoring", section on 'Optic neuropathy'.)

Not all case series distinguish between patients with a clinical presentation that suggests NAION versus those that are more consistent with a toxic neuropathy [147,148]. Another source of confusion is that patients taking amiodarone frequently have ischemic cardiac disease and therefore share risk factors with NAION [149]. Hence, the apparent relationship may represent confounding rather than causation. Because of the uncertainty surrounding the association, some suggest that for patients taking amiodarone who develop an optic neuropathy, the dose of amiodarone be lowered and/or discontinued if therapeutic alternatives exist [145-147].

Sympathomimetics — Case reports of NAION have been reported in which the onset of symptoms appeared to be related to the use of amphetamine or other sympathomimetic agent [150-152]. These agents are also associated with stroke and other cardiovascular complications. (See "Clinical diagnosis of stroke subtypes", section on 'Other risk factors'.)

Others

Blood loss — Vision loss in the setting of acute blood loss is often bilateral, but can be asymmetric and even strictly unilateral. When NAION occurs in this setting, the most frequent sources of bleeding are gastrointestinal tract in men and the uterus in women [153-156]. NAION has also been reported to be a complication of trauma requiring massive volume resuscitation [157,158].

Migraine — A few case reports have documented NAION occurring in migraineurs during an episode of migraine [159,160]. Vasospasm may underlie such cases [22,23].

Carotid dissection — An ischemic optic neuropathy is a rare complication of carotid dissection, occurring in 3 to 4 percent of cases, always in the setting of other clinical signs and symptoms [161,162]. In contrast to atherosclerotic carotid disease, which is not believed to be associated with NAION, carotid dissection can cause abrupt rather than slowly progressive carotid occlusion and loss of distal perfusion.

Genetic factors — Families with a strong predisposition to NAION have been described [119,163,164]. These cases are somewhat atypical. A survey of 79 individuals with NAION revealed a family history of NAION in a first-degree relative in four [165]. Investigators have sought to associate the mitochondrial mutations associated with Leber hereditary optic neuropathy (LHON) with NAION. None of the affected individuals among three families with NAION had one of the major LHON mutations [163]. These were also not observed in another investigation of 19 patients without known family history [166]. However, in the latter study and in another family with NAION, intermediate or secondary LHON mutations were more common in NAION patients compared with controls [164,166].

Metabolic factors — One study found elevated plasma homocysteine and lipoprotein(a) levels, as well as low vitamin B6 levels in 85 patients with new-onset NAION compared with 107 healthy controls, suggesting that these factors may increase the risk for developing NAION [167].

Infection — Several case reports have documented varicella zoster infection in association with ischemic optic neuropathy in patients who were suspected of having giant cell arteritis [168-171]. Whether the virus can also trigger an inflammatory optic neuropathy and whether it plays a pathogenic role in the development of temporal arteritis remains under investigation.

SUMMARY

Epidemiology – Nonarteritic anterior ischemic optic neuropathy (NAION) is an idiopathic, ischemic insult of the optic nerve head and is the most common form of optic neuropathy in older adults.

Older White adults (greater than 45 to 50 years) are most at risk of NAION. Males and females are affected approximately equally. (See 'Epidemiology' above.)

Pathogenesis – NAION is believed to result from vascular insufficiency of the optic nerve head. While atherosclerotic risk factors are prevalent in these patients, an underlying vasculopathy involving the optic nerve circulation has not been defined. A possible alternative or contributory mechanism involves a compartment syndrome affecting the optic nerve head. (See 'Pathogenesis' above.)

Etiologies and risk factors

Atherosclerosis – Most cases of NAION occur apparently spontaneously in older adults with vascular risk factors (diabetes, hypertension). (See 'Atherosclerosis' above.)

Small optic cup – A small optic cup, implying optic nerve fiber crowding, is a common finding in the fellow eye in patients with NAION and is believed to place individuals at risk for NAION. (See 'Ocular risk factors' above.)

Others – NAION has been described in other clinical settings that are believed to play a role in its onset in specific cases (table 1). (See 'Etiology and risk factors' above.)

  1. Rucker JC, Biousse V, Newman NJ. Ischemic optic neuropathies. Curr Opin Neurol 2004; 17:27.
  2. Salvetat ML, Pellegrini F, Spadea L, et al. Non-Arteritic Anterior Ischemic Optic Neuropathy (NA-AION): A Comprehensive Overview. Vision (Basel) 2023; 7.
  3. Mackenzie PJ, Cioffi GA. Vascular anatomy of the optic nerve head. Can J Ophthalmol 2008; 43:308.
  4. Baig MN, Lubow M, Immesoete P, et al. Vision loss after spine surgery: review of the literature and recommendations. Neurosurg Focus 2007; 23:E15.
  5. Hayreh SS. The 1994 Von Sallman Lecture. The optic nerve head circulation in health and disease. Exp Eye Res 1995; 61:259.
  6. Arnold AC. Pathogenesis of nonarteritic anterior ischemic optic neuropathy. J Neuroophthalmol 2003; 23:157.
  7. Guyer DR, Miller NR, Auer CL, Fine SL. The risk of cerebrovascular and cardiovascular disease in patients with anterior ischemic optic neuropathy. Arch Ophthalmol 1985; 103:1136.
  8. Characteristics of patients with nonarteritic anterior ischemic optic neuropathy eligible for the Ischemic Optic Neuropathy Decompression Trial. Arch Ophthalmol 1996; 114:1366.
  9. Johnson LN, Arnold AC. Incidence of nonarteritic and arteritic anterior ischemic optic neuropathy. Population-based study in the state of Missouri and Los Angeles County, California. J Neuroophthalmol 1994; 14:38.
  10. Hattenhauer MG, Leavitt JA, Hodge DO, et al. Incidence of nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1997; 123:103.
  11. Lee JY, Park KA, Oh SY. Prevalence and incidence of non-arteritic anterior ischaemic optic neuropathy in South Korea: a nationwide population-based study. Br J Ophthalmol 2018; 102:936.
  12. Hayreh SS, Zimmerman MB. Optic disc edema in non-arteritic anterior ischemic optic neuropathy. Graefes Arch Clin Exp Ophthalmol 2007; 245:1107.
  13. Preechawat P, Bruce BB, Newman NJ, Biousse V. Anterior ischemic optic neuropathy in patients younger than 50 years. Am J Ophthalmol 2007; 144:953.
  14. Hayreh SS. Anterior ischemic optic neuropathy. Arch Neurol 1981; 38:675.
  15. Tesser RA, Niendorf ER, Levin LA. The morphology of an infarct in nonarteritic anterior ischemic optic neuropathy. Ophthalmology 2003; 110:2031.
  16. Knox DL, Kerrison JB, Green WR. Histopathologic studies of ischemic optic neuropathy. Trans Am Ophthalmol Soc 2000; 98:203.
  17. Fry CL, Carter JE, Kanter MC, et al. Anterior ischemic optic neuropathy is not associated with carotid artery atherosclerosis. Stroke 1993; 24:539.
  18. Müller M, Kessler C, Wessel K, et al. Low-tension glaucoma: a comparative study with retinal ischemic syndromes and anterior ischemic optic neuropathy. Ophthalmic Surg 1993; 24:835.
  19. Arnold AC, Hepler RS, Hamilton DR, Lufkin RB. Magnetic resonance imaging of the brain in nonarteritic ischemic optic neuropathy. J Neuroophthalmol 1995; 15:158.
  20. Arnold AC, Hepler RS. Fluorescein angiography in acute nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1994; 117:222.
  21. Arnold AC, Badr MA, Hepler RS. Fluorescein angiography in nonischemic optic disc edema. Arch Ophthalmol 1996; 114:293.
  22. Hayreh SS, Piegors DJ, Heistad DD. Serotonin-induced constriction of ocular arteries in atherosclerotic monkeys. Implications for ischemic disorders of the retina and optic nerve head. Arch Ophthalmol 1997; 115:220.
  23. Kaiser HJ, Flammer J, Messerli J. Vasospasm: a risk factor for nonarteritic anterior ischemic optic neuropathy? Neuro-ophthalmology 1996; 16:5.
  24. Levin LA, Danesh-Meyer HV. Hypothesis: a venous etiology for nonarteritic anterior ischemic optic neuropathy. Arch Ophthalmol 2008; 126:1582.
  25. Jacobson DM, Vierkant RA, Belongia EA. Nonarteritic anterior ischemic optic neuropathy. A case-control study of potential risk factors. Arch Ophthalmol 1997; 115:1403.
  26. Hayreh SS, Joos KM, Podhajsky PA, Long CR. Systemic diseases associated with nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol 1994; 118:766.
  27. Salomon O, Huna-Baron R, Kurtz S, et al. Analysis of prothrombotic and vascular risk factors in patients with nonarteritic anterior ischemic optic neuropathy. Ophthalmology 1999; 106:739.
  28. Hayreh SS, Zimmerman MB, Podhajsky P, Alward WL. Nocturnal arterial hypotension and its role in optic nerve head and ocular ischemic disorders. Am J Ophthalmol 1994; 117:603.
  29. Chung SM, Gay CA, McCrary JA 3rd. Nonarteritic ischemic optic neuropathy. The impact of tobacco use. Ophthalmology 1994; 101:779.
  30. Deramo VA, Sergott RC, Augsburger JJ, et al. Ischemic optic neuropathy as the first manifestation of elevated cholesterol levels in young patients. Ophthalmology 2003; 110:1041.
  31. Giuffre G. Hematologic risk factors for anterior ischemic optic neuropathy. Neuro-ophthalmology 1990; 10:197.
  32. Talks SJ, Chong NH, Gibson JM, Dodson PM. Fibrinogen, cholesterol and smoking as risk factors for non-arteritic anterior ischaemic optic neuropathy. Eye (Lond) 1995; 9 ( Pt 1):85.
  33. Hayreh SS, Jonas JB, Zimmerman MB. Nonarteritic anterior ischemic optic neuropathy and tobacco smoking. Ophthalmology 2007; 114:804.
  34. Hayreh SS. Duke-elder lecture. Systemic arterial blood pressure and the eye. Eye (Lond) 1996; 10 ( Pt 1):5.
  35. Hayreh SS. Acute ischemic disorders of the optic nerve: Pathogenesis, Clinical Manifestations and Management. Ophthalmol Clin North Am 1996; 9:407.
  36. Hayreh SS. Role of nocturnal arterial hypotension in the development of ocular manifestations of systemic arterial hypertension. Curr Opin Ophthalmol 1999; 10:474.
  37. Hayreh SS, Podhajsky PA, Zimmerman B. Nonarteritic anterior ischemic optic neuropathy: time of onset of visual loss. Am J Ophthalmol 1997; 124:641.
  38. Hayreh SS, Podhajsky P, Zimmerman MB. Role of nocturnal arterial hypotension in optic nerve head ischemic disorders. Ophthalmologica 1999; 213:76.
  39. Hayreh SS, Podhajsky P, Zimmerman MB. Beta-blocker eyedrops and nocturnal arterial hypotension. Am J Ophthalmol 1999; 128:301.
  40. Landau K, Winterkorn JM, Mailloux LU, et al. 24-hour blood pressure monitoring in patients with anterior ischemic optic neuropathy. Arch Ophthalmol 1996; 114:570.
  41. Biousse V. Coagulation abnormalities and their neuro-ophthalmologic manifestations. Curr Opin Ophthalmol 1999; 10:382.
  42. Acheson JF, Sanders MD. Coagulation abnormalities in ischaemic optic neuropathy. Eye (Lond) 1994; 8 ( Pt 1):89.
  43. Worrall BB, Moazami G, Odel JG, Behrens MM. Anterior ischemic optic neuropathy and activated protein C resistance. A case report and review of the literature. J Neuroophthalmol 1997; 17:162.
  44. Srinivasan S, Fern A, Watson WH, McColl MD. Reversal of nonarteritic anterior ischemic optic neuropathy associated with coexisting primary antiphospholipid syndrome and Factor V Leiden mutation. Am J Ophthalmol 2001; 131:671.
  45. Sinnreich M, Rossillion B, Landis T, et al. Bilateral optic ischemic neuropathy related to chronic hepatitis C-associated anticardiolipin antibodies. Eur Neurol 2003; 49:243.
  46. Papageorgiou E, Karamagkiolis S, Dimera V. Nonarteritic anterior ischemic optic neuropathy and double thrombophilic defect: a new observation. Case Rep Ophthalmol 2012; 3:61.
  47. Weger M, Stanger O, Deutschmann H, et al. Hyperhomocyst(e)inaemia, but not MTHFR C677T mutation, as a risk factor for non-arteritic ischaemic optic neuropathy. Br J Ophthalmol 2001; 85:803.
  48. Pianka P, Almog Y, Man O, et al. Hyperhomocystinemia in patients with nonarteritic anterior ischemic optic neuropathy, central retinal artery occlusion, and central retinal vein occlusion. Ophthalmology 2000; 107:1588.
  49. Kawasaki A, Purvin VA, Burgett RA. Hyperhomocysteinaemia in young patients with non-arteritic anterior ischaemic optic neuropathy. Br J Ophthalmol 1999; 83:1287.
  50. Biousse V, Kerrison JB, Newman NJ. Is non-arteritic anterior ischaemic optic neuropathy related to homocysteine? Br J Ophthalmol 2000; 84:555.
  51. Nagy V, Facsko A, Takacs L, et al. Activated protein C resistance in anterior ischaemic optic neuropathy. Acta Ophthalmol Scand 2004; 82:140.
  52. Salomon O, Rosenberg N, Steinberg DM, et al. Nonarteritic anterior ischemic optic neuropathy is associated with a specific platelet polymorphism located on the glycoprotein Ibalpha gene. Ophthalmology 2004; 111:184.
  53. Kuhli-Hattenbach C, Scharrer I, Lüchtenberg M, Hattenbach LO. Selective thrombophilia screening of patients with nonarteritic anterior ischemic optic neuropathy. Graefes Arch Clin Exp Ophthalmol 2009; 247:485.
  54. Feit RH, Tomsak RL, Ellenberger C Jr. Structural factors in the pathogenesis of ischemic optic neuropathy. Am J Ophthalmol 1984; 98:105.
  55. Beck RW, Savino PJ, Repka MX, et al. Optic disc structure in anterior ischemic optic neuropathy. Ophthalmology 1984; 91:1334.
  56. Doro S, Lessell S. Cup-disc ratio and ischemic optic neuropathy. Arch Ophthalmol 1985; 103:1143.
  57. Saito H, Tomidokoro A, Tomita G, et al. Optic disc and peripapillary morphology in unilateral nonarteritic anterior ischemic optic neuropathy and age- and refraction-matched normals. Ophthalmology 2008; 115:1585.
  58. Contreras I, Rebolleda G, Noval S, Muñoz-Negrete FJ. Optic disc evaluation by optical coherence tomography in nonarteritic anterior ischemic optic neuropathy. Invest Ophthalmol Vis Sci 2007; 48:4087.
  59. Purvin V, King R, Kawasaki A, Yee R. Anterior ischemic optic neuropathy in eyes with optic disc drusen. Arch Ophthalmol 2004; 122:48.
  60. Jonas JB, Gusek GC, Naumann GO. Anterior ischemic optic neuropathy: nonarteritic form in small and giant cell arteritis in normal sized optic discs. Int Ophthalmol 1988; 12:119.
  61. Lee MS, Rizzo JF 3rd, Lessell S. Neuro-ophthalmologic complications of cataract surgery. Semin Ophthalmol 2002; 17:149.
  62. McCulley TJ, Lam BL, Feuer WJ. Incidence of nonarteritic anterior ischemic optic neuropathy associated with cataract extraction. Ophthalmology 2001; 108:1275.
  63. Hayreh SS. Anterior ischemic optic neuropathy. IV. Occurrence after cataract extraction. Arch Ophthalmol 1980; 98:1410.
  64. McCulley TJ, Lam BL, Feuer WJ. Nonarteritic anterior ischemic optic neuropathy and surgery of the anterior segment: temporal relationship analysis. Am J Ophthalmol 2003; 136:1171.
  65. Lam BL, Jabaly-Habib H, Al-Sheikh N, et al. Risk of non-arteritic anterior ischaemic optic neuropathy (NAION) after cataract extraction in the fellow eye of patients with prior unilateral NAION. Br J Ophthalmol 2007; 91:585.
  66. Lee AG, Kohnen T, Ebner R, et al. Optic neuropathy associated with laser in situ keratomileusis. J Cataract Refract Surg 2000; 26:1581.
  67. Cameron BD, Saffra NA, Strominger MB. Laser in situ keratomileusis-induced optic neuropathy. Ophthalmology 2001; 108:660.
  68. Slavin ML, Margulis M. Anterior ischemic optic neuropathy following acute angle-closure glaucoma. Arch Ophthalmol 2001; 119:1215.
  69. Mojon DS, Hedges TR 3rd, Ehrenberg B, et al. Association between sleep apnea syndrome and nonarteritic anterior ischemic optic neuropathy. Arch Ophthalmol 2002; 120:601.
  70. Palombi K, Renard E, Levy P, et al. Non-arteritic anterior ischaemic optic neuropathy is nearly systematically associated with obstructive sleep apnoea. Br J Ophthalmol 2006; 90:879.
  71. Young T, Shahar E, Nieto FJ, et al. Predictors of sleep-disordered breathing in community-dwelling adults: the Sleep Heart Health Study. Arch Intern Med 2002; 162:893.
  72. Li J, McGwin G Jr, Vaphiades MS, Owsley C. Non-arteritic anterior ischaemic optic neuropathy and presumed sleep apnoea syndrome screened by the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ). Br J Ophthalmol 2007; 91:1524.
  73. Mojon DS, Mathis J, Zulauf M, et al. Optic neuropathy associated with sleep apnea syndrome. Ophthalmology 1998; 105:874.
  74. Behbehani R, Mathews MK, Sergott RC, Savino PJ. Nonarteritic anterior ischemic optic neuropathy in patients with sleep apnea while being treated with continuous positive airway pressure. Am J Ophthalmol 2005; 139:518.
  75. Servilla KS, Groggel GC. Anterior ischemic optic neuropathy as a complication of hemodialysis. Am J Kidney Dis 1986; 8:61.
  76. Jackson TL, Farmer CK, Kingswood C, Vickers S. Hypotensive ischemic optic neuropathy and peritoneal dialysis. Am J Ophthalmol 1999; 128:109.
  77. Michaelson C, Behrens M, Odel J. Bilateral anterior ischaemic optic neuropathy associated with optic disc drusen and systemic hypotension. Br J Ophthalmol 1989; 73:762.
  78. Haider S, Astbury NJ, Hamilton DV. Optic neuropathy in uraemic patients on dialysis. Eye (Lond) 1993; 7 ( Pt 1):148.
  79. Korzets A, Marashek I, Schwartz A, et al. Ischemic optic neuropathy in dialyzed patients: a previously unrecognized manifestation of calcific uremic arteriolopathy. Am J Kidney Dis 2004; 44:e93.
  80. Basile C, Addabbo G, Montanaro A. Anterior ischemic optic neuropathy and dialysis: role of hypotension and anemia. J Nephrol 2001; 14:420.
  81. Winkelmayer WC, Eigner M, Berger O, et al. Optic neuropathy in uremia: an interdisciplinary emergency. Am J Kidney Dis 2001; 37:E23.
  82. Kim JS, Deputy S, Vives MT, Aviles DH. Sudden blindness in a child with end-stage renal disease. Pediatr Nephrol 2004; 19:691.
  83. Lapeyraque AL, Haddad E, André JL, et al. Sudden blindness caused by anterior ischemic optic neuropathy in 5 children on continuous peritoneal dialysis. Am J Kidney Dis 2003; 42:E3.
  84. Chutorian AM, Winterkorn JM, Geffner M. Anterior ischemic optic neuropathy in children: case reports and review of the literature. Pediatr Neurol 2002; 26:358.
  85. Levy J, Tovbin D, Lifshitz T, et al. Intraocular pressure during haemodialysis: a review. Eye (Lond) 2005; 19:1249.
  86. Knox DL, Hanneken AM, Hollows FC, et al. Uremic optic neuropathy. Arch Ophthalmol 1988; 106:50.
  87. Korzets Z, Zeltzer E, Rathaus M, et al. Uremic optic neuropathy. A uremic manifestation mandating dialysis. Am J Nephrol 1998; 18:240.
  88. Lee LA, Roth S, Posner KL, et al. The American Society of Anesthesiologists Postoperative Visual Loss Registry: analysis of 93 spine surgery cases with postoperative visual loss. Anesthesiology 2006; 105:652.
  89. Myers MA, Hamilton SR, Bogosian AJ, et al. Visual loss as a complication of spine surgery. A review of 37 cases. Spine (Phila Pa 1976) 1997; 22:1325.
  90. Stevens WR, Glazer PA, Kelley SD, et al. Ophthalmic complications after spinal surgery. Spine (Phila Pa 1976) 1997; 22:1319.
  91. Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol 2008; 145:604.
  92. Worrell L, Rowe M, Petti G. Amaurosis: a complication of bilateral radical neck dissection. Am J Otolaryngol 2002; 23:56.
  93. Balm AJ, Brown DH, De Vries WA, Snow GB. Blindness: a potential complication of bilateral neck dissection. J Laryngol Otol 1990; 104:154.
  94. Marks SC, Jaques DA, Hirata RM, Saunders JR Jr. Blindness following bilateral radical neck dissection. Head Neck 1990; 12:342.
  95. Wilson JF, Freeman SB, Breene DP. Anterior ischemic optic neuropathy causing blindness in the head and neck surgery patient. Arch Otolaryngol Head Neck Surg 1991; 117:1304.
  96. Suárez-Fernández MJ, Clariana-Martín A, Mencía-Gutiérrez E, et al. Bilateral anterior ischemic optic neuropathy after bilateral neck dissection. Clin Ophthalmol 2010; 4:95.
  97. Sadaba LM, Garcia-Layana A, Maldonado MJ, Berian JM. Bilateral ischemic optic neuropathy after transurethral prostatic resection: a case report. BMC Ophthalmol 2006; 6:32.
  98. Gilbert ME, Savino PJ, Sergott RC. Anterior ischaemic optic neuropathy after rotator cuff surgery. Br J Ophthalmol 2006; 90:248.
  99. Dunker S, Hsu HY, Sebag J, Sadun AA. Perioperative risk factors for posterior ischemic optic neuropathy. J Am Coll Surg 2002; 194:705.
  100. Janicki PK, Pai R, Kelly Wright J, et al. Ischemic optic neuropathy after liver transplantation. Anesthesiology 2001; 94:361.
  101. Kalyani SD, Miller NR, Dong LM, et al. Incidence of and risk factors for perioperative optic neuropathy after cardiac surgery. Ann Thorac Surg 2004; 78:34.
  102. Nuttall GA, Garrity JA, Dearani JA, et al. Risk factors for ischemic optic neuropathy after cardiopulmonary bypass: a matched case/control study. Anesth Analg 2001; 93:1410.
  103. Shapira OM, Kimmel WA, Lindsey PS, Shahian DM. Anterior ischemic optic neuropathy after open heart operations. Ann Thorac Surg 1996; 61:660.
  104. Sweeney PJ, Breuer AC, Selhorst JB, et al. Ischemic optic neuropathy: a complication of cardiopulmonary bypass surgery. Neurology 1982; 32:560.
  105. Chang SH, Miller NR. The incidence of vision loss due to perioperative ischemic optic neuropathy associated with spine surgery: the Johns Hopkins Hospital Experience. Spine (Phila Pa 1976) 2005; 30:1299.
  106. Warner ME, Warner MA, Garrity JA, et al. The frequency of perioperative vision loss. Anesth Analg 2001; 93:1417.
  107. Buono LM, Foroozan R. Perioperative posterior ischemic optic neuropathy: review of the literature. Surv Ophthalmol 2005; 50:15.
  108. Moster ML. Visual loss after coronary artery bypass surgery. Surv Ophthalmol 1998; 42:453.
  109. Margheritini F, Camillieri G, Mancini L, Mariani PP. C-reactive protein and erythrocyte sedimentation rate changes following arthroscopically assisted anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc 2001; 9:343.
  110. Sha'aban RI, Asfour WM. Visual loss after coronary artery bypass surgery. Saudi Med J 2000; 21:90.
  111. Dilger JA, Tetzlaff JE, Bell GR, et al. Ischaemic optic neuropathy after spinal fusion. Can J Anaesth 1998; 45:63.
  112. Alexandrakis G, Lam BL. Bilateral posterior ischemic optic neuropathy after spinal surgery. Am J Ophthalmol 1999; 127:354.
  113. Delattre O, Thoreux P, Liverneaux P, et al. Spinal surgery and ophthalmic complications: a French survey with review of 17 cases. J Spinal Disord Tech 2007; 20:302.
  114. Strome SE, Hill JS, Burnstine MA, et al. Anterior ischemic optic neuropathy following neck dissection. Head Neck 1997; 19:148.
  115. Pomeranz HD, Bhavsar AR. Nonarteritic ischemic optic neuropathy developing soon after use of sildenafil (viagra): a report of seven new cases. J Neuroophthalmol 2005; 25:9.
  116. Cunningham AV, Smith KH. Anterior ischemic optic neuropathy associated with viagra. J Neuroophthalmol 2001; 21:22.
  117. Pomeranz HD, Smith KH, Hart WM Jr, Egan RA. Sildenafil-associated nonarteritic anterior ischemic optic neuropathy. Ophthalmology 2002; 109:584.
  118. Tarantini A, Faraoni A, Menchini F, Lanzetta P. Bilateral simultaneous nonarteritic anterior ischemic optic neuropathy after ingestion of sildenafil for erectile dysfunction. Case Rep Med 2012; 2012:747658.
  119. Felekis T, Asproudis I, Katsanos K, Tsianos E. A case of nonarteritic anterior ischemic optic neuropathy of a male with family history of the disease after receiving sildenafil. Clin Ophthalmol 2011; 5:1443.
  120. Moschos MM, Margetis I. Bilateral simultaneous anterior ischemic optic neuropathy associated with sildenafil. Case Rep Ophthalmol 2011; 2:262.
  121. Campbell UB, Walker AM, Gaffney M, et al. Acute nonarteritic anterior ischemic optic neuropathy and exposure to phosphodiesterase type 5 inhibitors. J Sex Med 2015; 12:139.
  122. Flahavan EM, Li H, Gupte-Singh K, et al. Prospective Case-crossover Study Investigating the Possible Association Between Nonarteritic Anterior Ischemic Optic Neuropathy and Phosphodiesterase Type 5 Inhibitor Exposure. Urology 2017; 105:76.
  123. Hayreh SS. Erectile dysfunction drugs and non-arteritic anterior ischemic optic neuropathy: is there a cause and effect relationship? J Neuroophthalmol 2005; 25:295.
  124. Liu B, Zhu L, Zhong J, et al. The Association Between Phosphodiesterase Type 5 Inhibitor Use and Risk of Non-Arteritic Anterior Ischemic Optic Neuropathy: A Systematic Review and Meta-Analysis. Sex Med 2018; 6:185.
  125. Nathoo NA, Etminan M, Mikelberg FS. Association between phosphodiesterase-5 inhibitors and nonarteritic anterior ischemic optic neuropathy. J Neuroophthalmol 2015; 35:12.
  126. Sivaswamy L, Vanstavern GP. Ischemic optic neuropathy in a child. Pediatr Neurol 2007; 37:371.
  127. http://www.fda.gov/cder/consumerinfo/viagra/vIAGRA.htm (Accessed on July 11, 2005).
  128. Bollinger K, Lee MS. Recurrent visual field defect and ischemic optic neuropathy associated with tadalafil rechallenge. Arch Ophthalmol 2005; 123:400.
  129. Pepin S, Pitha-Rowe I. Stepwise decline in visual field after serial sildenafil use. J Neuroophthalmol 2008; 28:76.
  130. McCulley TJ, Lam BL, Marmor MF, et al. Acute effects of sildenafil (viagra) on blue-on-yellow and white-on-white Humphrey perimetry. J Neuroophthalmol 2000; 20:227.
  131. Sponsel WE, Paris G, Sandoval SS, et al. Sildenafil and ocular perfusion. N Engl J Med 2000; 342:1680.
  132. Grunwald JE, Siu KK, Jacob SS, Dupont J. Effect of sildenafil citrate (Viagra) on the ocular circulation. Am J Ophthalmol 2001; 131:751.
  133. Grunwald JE, Metelitsina T, Grunwald L. Effect of sildenafil citrate (Viagra) on retinal blood vessel diameter. Am J Ophthalmol 2002; 133:809.
  134. Pache M, Meyer P, Prünte C, et al. Sildenafil induces retinal vasodilatation in healthy subjects. Br J Ophthalmol 2002; 86:156.
  135. McGwin G Jr, Vaphiades MS, Hall TA, Owsley C. Non-arteritic anterior ischaemic optic neuropathy and the treatment of erectile dysfunction. Br J Ophthalmol 2006; 90:154.
  136. A Study to Assess Whether PDE5 Inhibitors Increase the Chance of Triggering the Onset of Acute NAION. http://www.clinicaltrials.gov/ct2/show/NCT00759174?term=naion&rank=1) (Accessed on June 06, 2013).
  137. Lohmann CP, Kroher G, Bogenrieder T, et al. Severe loss of vision during adjuvant interferon alfa-2b treatment for malignant melanoma. Lancet 1999; 353:1326.
  138. Purvin VA. Anterior ischemic optic neuropathy secondary to interferon alfa. Arch Ophthalmol 1995; 113:1041.
  139. Vardizer Y, Linhart Y, Loewenstein A, et al. Interferon-alpha-associated bilateral simultaneous ischemic optic neuropathy. J Neuroophthalmol 2003; 23:256.
  140. Chan JW. Bilateral non-arteritic ischemic optic neuropathy associated with pegylated interferon for chronic hepatitis C. Eye (Lond) 2007; 21:877.
  141. Sene D, Touitou V, Bodaghi B, et al. Intraocular complications of IFN-alpha and ribavirin therapy in patients with chronic viral hepatitis C. World J Gastroenterol 2007; 13:3137.
  142. Berg KT, Nelson B, Harrison AR, et al. Pegylated interferon alpha-associated optic neuropathy. J Neuroophthalmol 2010; 30:117.
  143. Seddik H, Tamzaourte M, Rouibaa F, et al. Irreversible anterior ischemic optic neuropathy complicating interferon alpha and ribaverin therapy. Int J Hepatol 2011; 2011:814242.
  144. Chen D, Hedges TR. Amiodarone optic neuropathy--review. Semin Ophthalmol 2003; 18:169.
  145. Murphy MA, Murphy JF. Amiodarone and optic neuropathy: the heart of the matter. J Neuroophthalmol 2005; 25:232.
  146. Macaluso DC, Shults WT, Fraunfelder FT. Features of amiodarone-induced optic neuropathy. Am J Ophthalmol 1999; 127:610.
  147. Purvin V, Kawasaki A, Borruat FX. Optic neuropathy in patients using amiodarone. Arch Ophthalmol 2006; 124:696.
  148. Mäntyjärvi M, Tuppurainen K, Ikäheimo K. Ocular side effects of amiodarone. Surv Ophthalmol 1998; 42:360.
  149. Nagra PK, Foroozan R, Savino PJ, et al. Amiodarone induced optic neuropathy. Br J Ophthalmol 2003; 87:420.
  150. Fivgas GD, Newman NJ. Anterior ischemic optic neuropathy following the use of a nasal decongestant. Am J Ophthalmol 1999; 127:104.
  151. Chan JW. Acute nonarteritic ischaemic optic neuropathy after phentermine. Eye (Lond) 2005; 19:1238.
  152. Wijaya J, Salu P, Leblanc A, Bervoets S. Acute unilateral visual loss due to a single intranasal methamphetamine abuse. Bull Soc Belge Ophtalmol 1999; 271:19.
  153. Johnson MW, Kincaid MC, Trobe JD. Bilateral retrobulbar optic nerve infarctions after blood loss and hypotension. A clinicopathologic case study. Ophthalmology 1987; 94:1577.
  154. Hayreh SS. Anterior ischemic optic neuropathy. VIII. Clinical features and pathogenesis of post-hemorrhagic amaurosis. Ophthalmology 1987; 94:1488.
  155. Ballen PH, Fox MJ, Weissman GS. Ischemic optic neuropathy secondary to intestinal hemorrhage. Ann Ophthalmol 1985; 17:486.
  156. Foroozan R, Buono LM, Savino PJ. Optic disc structure and shock-induced anterior ischemic optic neuropathy. Ophthalmology 2003; 110:327.
  157. Cullinane DC, Jenkins JM, Reddy S, et al. Anterior ischemic optic neuropathy: a complication after systemic inflammatory response syndrome. J Trauma 2000; 48:381.
  158. Shaked G, Gavriel A, Roy-Shapira A. Anterior ischemic optic neuropathy after hemorrhagic shock. J Trauma 1998; 44:923.
  159. Weinstein JM, Feman SS. Ischemic optic neuropathy in migraine. Arch Ophthalmol 1982; 100:1097.
  160. Katz B. Bilateral sequential migrainous ischemic optic neuropathy. Am J Ophthalmol 1985; 99:489.
  161. Biousse V, Schaison M, Touboul PJ, et al. Ischemic optic neuropathy associated with internal carotid artery dissection. Arch Neurol 1998; 55:715.
  162. Baumgartner RW, Bogousslavsky J. Clinical manifestations of carotid dissection. Front Neurol Neurosci 2005; 20:70.
  163. Hayreh SS, Fingert JH, Stone E, Jacobson DM. Familial non-arteritic anterior ischemic optic neuropathy. Graefes Arch Clin Exp Ophthalmol 2008; 246:1295.
  164. Fingert JH, Grassi MA, Janutka JC, et al. Mitochondrial variant G4132A is associated with familial non-arteritic anterior ischemic optic neuropathy in one large pedigree. Ophthalmic Genet 2007; 28:1.
  165. Wang MY, Sadun F, Levin LB, et al. Occurrence of familial nonarteritic anterior ischemic optic neuropathy in a case series. J Neuroophthalmol 1999; 19:144.
  166. Bosley TM, Abu-Amero KK, Ozand PT. Mitochondrial DNA nucleotide changes in non-arteritic ischemic optic neuropathy. Neurology 2004; 63:1305.
  167. Giambene B, Sodi A, Sofi F, et al. Evaluation of traditional and emerging cardiovascular risk factors in patients with non-arteritic anterior ischemic optic neuropathy: a case-control study. Graefes Arch Clin Exp Ophthalmol 2009; 247:693.
  168. Nagel MA, Bennett JL, Khmeleva N, et al. Multifocal VZV vasculopathy with temporal artery infection mimics giant cell arteritis. Neurology 2013; 80:2017.
  169. Nagel MA, Russman AN, Feit H, et al. VZV ischemic optic neuropathy and subclinical temporal artery infection without rash. Neurology 2013; 80:220.
  170. Salazar R, Russman AN, Nagel MA, et al. Varicella zoster virus ischemic optic neuropathy and subclinical temporal artery involvement. Arch Neurol 2011; 68:517.
  171. Mathias M, Nagel MA, Khmeleva N, et al. VZV multifocal vasculopathy with ischemic optic neuropathy, acute retinal necrosis and temporal artery infection in the absence of zoster rash. J Neurol Sci 2013; 325:180.
Topic 5233 Version 12.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟