Survey of Ophthalmology
Volume 56, Issue 1 , Pages 86-93, January 2011

Not Again!

  • Kathryn L. Pepple, MD, PhD

      Affiliations

    • Department of Ophthalmology, Duke University Eye Center and Duke University Medical Center, Durham, North Carolina, USA
    • ,
  • M. Tariq Bhatti, MD

      Affiliations

    • Department of Ophthalmology, Duke University Eye Center and Duke University Medical Center, Durham, North Carolina, USA
    • Department of Medicine (Division of Neurology), Duke University Eye Center and Duke University Medical Center, Durham, North Carolina, USA
    • Corresponding Author InformationReprint address: M. Tariq Bhatti, MD, 2351 Erwin Road, Duke University Eye Center, DUMC 3802, Durham, NC 27710-3802.
    • ,
  • Rod Foroozan, MD

      Affiliations

    • Cullen Eye Institute, Baylor College of Medicine, Houston, Texas, USA

published online 16 August 2010.

Peter Savino and Helen Danesh-Meyer, Editors

Article Outline

Abstract 

A 58-year-old white man presented with a second episode of vision loss in the same eye. Diagnostic evaluations conducted at each episode were unrevealing for an underlying etiology, and a presumptive diagnosis of recurrent non-arteritic anterior ischemic optic neuropathy (NAION) was made. The evaluation of recurrent NAION is discussed.

Key words: giant cell arteritis, ischemia, optic nerve head edema, optic neuropathy, recurrent

 

(In keeping with the format of a clinical pathologic conference, the abstract and key words appear at the end of the article.)

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Case Report 

A 58-year-old white man was referred for evaluation of optic nerve head (ONH) edema OD. Three months earlier, he had been seen by an ophthalmologist and neurologist because of superior visual field loss OD and inferior ONH edema (Fig. 1). At that time a complete blood count, Westergren erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), antinuclear antibodies, angiotensin converting enzyme level, rapid plasma reagin, Lyme titers, cranial and orbital magnetic resonance imaging (MRI) with contrast, and a lumbar puncture were all normal or negative. The diagnosis of non-arteritic anterior ischemic optic neuropathy (NAION) was made. The edema resolved within four weeks, and the superior visual field defect remained unchanged.

  • View full-size image.
  • Fig. 1 

    A: Fundus photograph taken at the time of the patient's first episode of vision loss OD. Despite the suboptimal quality of the photograph, inferior ONH edema is evident. B: Mid-to-late phase of intravenous fluorescein angiography demonstrates leakage of the inferior ONH. C: Static perimetry shows a superior altitudinal visual field defect.

Three days prior to presenting to our clinic the patient awoke and noticed a decrease in the inferior half of the vision OD. He also reported a dull ache behind the right eye. He denied headache, scalp tenderness, jaw claudication, fever, weight loss, Uhthoff's phenomenon, numbness, or weakness.

His past medical history was notable for thyroid disease, gastroesophageal reflux, and peptic ulcer disease. He was taking levothyroxine sodium, ranitidine, and a daily 325 mg enteric-coated aspirin. He denied use of phosphodiesterase-5 inhibitors. His past ocular history was notable for laser-assisted in situ keratomileusis surgery OU in 2000 and radial keratotomy OU in 1995. He denied tobacco use. His father was legally blind as the result of bilateral “eye strokes” that occurred 3 years apart.

Blood pressure was 146/55 mm Hg. Visual acuities were 20/40 OD and 20/20 OS. Intraocular pressures were 23 mm Hg OD and 18 mm Hg OS. Color vision was intact OU. Pupils were equal with a right relative afferent pupillary defect. The superficial temporal artery pulses were easily palpable and nontender. Slit-lamp biomicroscopy revealed scars from his refractive surgeries and mild nuclear sclerotic cataracts OU. There was superior ONH edema OD with a flame-shaped hemorrhage and inferior ONH pallor (Fig. 2A and 2B). The left optic nerve was normal with an absent cup (Fig. 2C). The remainder of the fundus examination was normal. Optical coherence tomography of the retinal nerve fiber layer (OCT-RNFL) revealed superior and nasal thickening and inferotemporal thinning OD (Fig. 2D). Static perimetry OD showed a dense superior altitudinal defect and an inferior arcuate defect (Fig. 2E).

  • View full-size image.
  • Fig. 2 

    A: Fundus photograph at the time of the second episode of vision loss OD shows superior ONH edema. B: A higher magnification image of the superior ONH. C: The left ONH is normal, but crowded. D: Static perimetry OD demonstrates a new inferior arcuate defect and stable superior altitudinal defect. E: OCT-RNFL OD shows superonasal thickening and inferotemporal thinning.

What are the diagnostic possibilities?

What work-up would you recommend?

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Comments 

Comments by Rod Foroozan, MD 

The initial episode of visual loss appears to have been typical NAION. He had acute visual loss, sectoral optic disk swelling with a small optic disk cup in the fellow eye, and a stable visual field defect with resolution of the optic disk edema after 1 month. Now he returns with recurrent optic disk edema on the same side with a new visual field defect.

Before considering the possible causes and tests for the optic neuropathy, some additional clinical details would be helpful. We do not know if there was pain with eye movement during either episode (a symptom more suggestive of an inflammatory optic neuropathy).57 We are also not told if there is evidence of intraocular inflammation, specifically, if there are cells in the vitreous. It would be helpful to know his height and weight to get an idea of his body mass index and ask about snoring or excessive daytime somnolence, as there is some evidence sleep apnea may be a risk factor for ischemic optic neuropathy.48 Although some vascular risk factors (elevated blood pressure) are noted, we do not know if he has a history of hyperlipidemia or coagulopathy, considered risk factors for NAION by some.16 I would suggest a fasting lipid profile if he has not had one recently. Unless there are other findings that suggest a coagulopathy, I do not screen for coagulation disorders in patients with NAION. There is no history of diabetes mellitus, but fasting blood sugar and hemoglobin A1c are helpful for asymptomatic patients. The family history of “eye strokes” is intriguing, and it may help to know if these were retinovascular occlusions or ischemic optic neuropathies; however, most retinovascular occlusions or ischemic optic neuropathies do not have an inherited basis. Furthermore, the clinical findings are not suggestive of Leber hereditary optic neuropathy (and I am not aware of a patient with Leber having recurrent optic disc edema in the same eye).

Although the cause of NAION remains unclear, most patients have a small optic disk cup that is believed to result in a compartment syndrome with the onset of ischemia. Some think that the resulting optic atrophy decreases the severity of the compartment syndrome thereby reducing the risk of recurrent optic neuropathy; others have questioned this hypothesis, however.28 Because non-arteritic anterior ischemic optic neuropathy typically occurs just once per eye, other types of optic neuropathy should be considered. The most frequent mimic of ischemic optic neuropathy is inflammatory optic neuropathy.57 Demyelination from multiple sclerosis is the most common cause of inflammatory optic neuropathy, but several other types may occur. These include sterile inflammation (sarcoidosis), infectious (syphilis), vasculitis (systemic lupus erythematous), and other autoimmune optic neuropathies.

I would suggest obtaining his prior records to review the blood tests and images of his initial MRI of the brain and orbits to ensure it was performed with fat suppression and to look for contrast enhancement of the optic nerve (much more characteristic for an inflammatory optic neuropathy than an ischemic56) and to ensure there were no white matter lesions. An MRI of the brain and orbits could be repeated—again, chiefly looking for optic nerve enhancement and white matter lesions suggestive of demyelination. I would order additional blood tests including: anti-neutrophil cytoplasmic antibody and fluorescent treponemal antibody absorbed, although in the absence of additional history or clinical findings I think the yield will be low. Likewise, at this point the likelihood of an autoimmune optic neuropathy is low, and while there is serologic testing for optic nerve antibodies, I would not order them at this time.

Although the clinical findings are not suggestive of a compressive optic neuropathy given optic disc edema followed by resolution and then recurrence of edema, AION can be mimicked by compressive lesions, including meningiomas.24 Occasionally CT may reveal calcification of the optic nerve sheath that can go undetected with MRI. There is little else to suggest a meningeal process or other involvement of the central nervous system, and I would not repeat the lumbar puncture.

Although there is no clinical suggestion of an arteritic anterior ischemic optic neuropathy (AAION), intravenous fluorescein angiography can be performed to look for vasculitis and impaired retinal/choroidal perfusion15 that would be more suggestive of AAION, and the ESR could be repeated. Recurrent NAION is uncommon, but has been noted in patients taking medications that may predispose to ischemic optic neuropathy.11 In giant cell arteritis it is commonly noted, both in untreated patients and those on corticosteroids.7, 41

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Case Report (Continued) 

A comprehensive metabolic panel and complete blood count was normal. ESR was 12 mm/hr and CRP was 0.36 mg/l. A lipid panel was normal. Fasting blood glucose was 124 mg/dl and glycated hemoglobin (HBA1c) was 6.0%. A hypercoaguability work up that included prothrombin gene mutation, Von Willebrand factor antigen, factor V Leiden, functional antithrombin III, functional protein C and S assays, anti-cardiolipin antibodies, homocystine, fibrinogen, prothrombin time, partial thromboplastin time, serum protein electrophoresis, and lupus anticoagulant panel was normal or negative. MRI of the brain and orbits with contrast and a MR angiography of the neck vessels were also normal.

What would you do next?

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Comments (Continued) 

Comments by Dr. Foroozan 

Despite all of these tests, and others that have not yet been performed, we may be left with only the clinical course to determine the cause of the optic neuropathy. Recurrent NAION may occur in 5% of patients with anterior ischemic optic neuropathy.6 If this is what this patient has, I would expect the optic disk edema to resolve spontaneously over the next several weeks or months, the visual function to remain generally stable, and the absence of other ocular findings such as intraocular inflammation. Recurrent NAION remains a diagnosis that is often best made retrospectively, after continued observation reveals no other cause or progression of findings. Reassessing vascular risk factors may be important, and if a sleep study has not been performed it may be helpful. Some believe that nocturnal hypotension is an important risk factor28 and blood-pressure monitoring may be useful.

The patients with recurrent NAION that I have seen have been similar to this patient in that the initial bout caused sectoral optic disc edema and subsequent optic disc pallor correlating to the area of prior edema. Perhaps this ischemic episode decompresses the optic disc in one sector but still leaves the unaffected portion of the optic disc at risk. The recurrent episode then involves the initially unaffected portion of the optic disk. When I have tried to test this theory reviewing prior reports, the evidence is limited, in part because many of the reports on recurrent NAION do not depict photographic evidence of the optic disk morphology. Furthermore this theory is not likely to explain patients who have been reported to have more than two (and even more than seven) recurrences of NAION in the same eye.31 Because I do not have the benefit of follow-up to know his visual outcome I would offer a course of corticosteroids empirically. Some types of optic neuropathy (typically inflammatory) may respond to corticosteroids—so that a brisk, robust improvement suggests a diagnosis other than NAION. Furthermore, there is some evidence to suggest that systemic corticosteroids may be helpful in patients with NAION.32 Accepting that the patient here has a mildly elevated blood sugar and blood pressure and that the corticosteroids may aggravate these conditions, I think there is little down-side to trying a short course here.

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Case Report (Continued) 

No intervention was undertaken. Two weeks later there was a decrease in the superior ONH swelling (Fig. 3B). Two months after the onset of symptoms, the right ONH swelling was completely resolved and was replaced with pallor (Fig. 3C). The visual field defect remained unchanged.

  • View full-size image.
  • Fig. 3 

    Serial optic nerve photographs (top) and OCT (bottom) at presentation A: 2-week follow-up B: and 2-month follow-up C: On initial evaluation, there is superior ONH edema with hemorrhage. At 2 weeks the superior ONH edema has decreased. By 2 months the ONH is pale without edema.

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Discussion 

NAION is ischemic injury to the ONH believed to be the result of a vasculopathy involving the posterior ciliary arteries (PCAs).29, 40 The exact mechanism leading to ischemia is unknown, but appears to be associated with several risk factors and conditions (Table 1).

Table 1. Risk Factors, Medications, and Conditions Associated with NAION
Anatomic FactorsSystemic Medical ConditionsOptic Nerve HypoperfusionMedicationsGenetic Predisposition
“Disk at risk”5, 17, 18, 47
Hyperopia51		DM, HTN, smoking34
OSA52
ESRD on hemodialysis3, 45
Prothrombotic conditions22, 23, 39, 43, 54, 62
-Hyperhomocysteinemia

-lupus anticoagulant

-antiphospholipid antibody syndrome

-factor V Leiden mutation

-protein C, S, and antithrombin III deficiencies

-Platelet glycoprotein polymorphisms (VNTR B allele of glycoprotein ib-alpha)

Nocturnal hypotension27, 33
Decreased carotid flow60
Spinal and cardiac surgery13, 49, 58		PDE5 inhibitors46, 53, 55
Interferon alpha9
Intravitreal avastin21
Amiodarone64
Oxymetazoline nasal spray20		Mitochondrial gene mutations12, 19
HLA-A2936
Oxadative stress1
-(GST) mutations

DM = diabetes mellitus; HTN = hypertension; OSA = obstructive sleep apnea; ESRD = end stage renal disease; PDE5 = phosphodiesterase type 5; HLA-A29 = human leukocyte antigen-A29; GST = glutathione S-transferase.

For patients with NAION, the risk of fellow eye involvement is 14.7% at 5 years; however, recurrence in the same eye is considered rare.50 In a study of 829 eyes with NAION, only 53 (6%) had a recurrence in the same eye.31 This low rate of recurrence is believed to be the result of axonal loss decompressing the ONH preventing a self-perpetuating edema and ischemic cascade. Another possible explanation of the low recurrent rate of NAION in the same eye is based on physiologic variations of the vascular supply to the ONH.28 The blood supply to the ONH is derived primarily from PCAs. The number of PCAs can vary from one to five, but normally two to three are present.26 Patients with fewer PCAs may be more susceptible to a second ischemic injury in watershed regions of the ONH.25

The lack of level I clinical evidence and the mixed results of level III, IV, and V studies has not confirmed a proven effective treatment for NAION.2 Currently, the management of NAION includes modification of underlying risk factors, treatment of any associated medical conditions, and attempts to reduce fellow-eye involvement. A few retrospective case series suggest aspirin may reduce the risk of fellow-eye involvement.4, 44, 59 Other studies have failed to show a protective effect of aspirin, and the long-term benefit of aspirin is unknown.40 The pharmacological effect of aspirin has been questioned because hypoperfusion and not thrombosis is believed to be the inciting mechanism in the majority of cases of NAION.29

Recently a prospective, non-randomized, evaluator-blinded study of oral systemic corticosteroids administered after the diagnosis of NAION was published.32 Treatment consisted of two weeks of 80 mg of oral prednisone followed by a slow taper over 2 months. The study found that of the group with visual acuity of 20/70 or worse treated within 2 weeks, 69.8% experienced visual improvement at 6 months. These treated eyes were compared to a natural history cohort in which only 40.5% improved at 6 months (p = 0.001) After 1 year when all patients treated with corticosteroids regardless of initial visual acuity or time of initiation of treatment were considered, 25.2% of patients demonstrated improvement in visual acuity and 63.3% were unchanged.32 This more inclusive treatment group was not compared to the natural history cohort.

A small number of studies investigating intravitreal corticosteroid injection in NAION have not demonstrated reproducible visual benefit, and this intervention carries the additional risk of compromising ONH perfusion pressure through transient elevation of intraocular pressure.37, 38, 63 Other medical therapies for NAION have only been reported as case reports and small series. In one such case report from Bennett et al, NAION was treated with a single injection of 1.25 mg/0.05 mL bevacizumab, a humanized monoclonal antibody targeted against vascular endothelial growth factor A. After 9 days the ONH edema was markedly reduced, and visual acuity had improved from count fingers to 20/100.8 Another small prospective study evaluated the effect of 100 mg levodopa/25 mg carbidopa given three times a day for 3 weeks within 45 days of NAION onset. There was a trend toward visual improvement in the treated group compared to the control group, but the results were not statistically significant.35

An interesting and novel aspect of NAION research focuses on exploring the role of mitochondrial mutations in disease pathogenesis. Fingert et al identified a sequence variation (G4132A) in the mitochondrial gene NADH dehydrogenase subunit 1 (ND1) in six members of a familial NAION pedigree.19 Bosley et al sequenced the complete mitochondrial genome in 19 patients with NAION and identified more nonsynonymous nucleotide changes in NAION patients than in controls.12 These studies raise the possibility that in certain cases metabolic injury instead of—or in addition to—ischemic injury may play a primary role in the pathogenesis of NAION. In contrast to these studies, Hayreh et al found that the G4132A variant of the ND1 gene was not associated with non-familial NAION and was not identified in two additional pedigrees of familial NAION.30

The development of NAION animal models offers the hope of expanding our understanding of the basic science of the disease, and the development of future therapeutic options.10, 61 The rodent model of NAION suggests that inflammation may play an important role in the damage to the ONH after the initial ischemic event.65 Zhang et al demonstrated that 1 day after photochemically inducing ischemic injury to the ONH, there was infiltration of macrophages within the nerve, persisting up to 14 days from the time of injury.65 At this time, it is not clear if this inflammatory response is detrimental by perpetuating inflammation resulting in additional edema and optic nerve ischemia, or beneficial by promoting the healing process.42 The recent development of a primate model of NAION will be very useful in exploring these questions, and extrapolating effective therapies from basic science advances.14

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Disclosure 

The authors reported no proprietary or commercial interest in any product mentioned or concept discussed in this article.

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References 

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PII: S0039-6257(10)00111-6

doi:10.1016/j.survophthal.2010.05.002

Survey of Ophthalmology
Volume 56, Issue 1 , Pages 86-93, January 2011

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