Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
INTRODUCTION — Optic neuritis is an inflammatory, demyelinating condition that causes acute, usually monocular, visual loss. It is highly associated with multiple sclerosis (MS). Optic neuritis is the presenting feature of MS in 15 to 20 percent of patients and occurs in 50 percent at some time during the course of their illness [1-4].
The term optic neuritis is sometimes applied to other inflammatory and infectious conditions affecting the optic nerve. These and other causes of optic neuropathy are discussed separately. (See "Optic neuropathies".)
The epidemiology, pathophysiology, clinical features, and diagnosis of demyelinating optic neuritis will be covered here. Prognosis and treatment of optic neuritis and other clinical manifestations of multiple sclerosis are discussed separately. (See "Optic neuritis: Prognosis and treatment" and "Clinical features of multiple sclerosis in adults" and "Clinically isolated syndromes suggestive of multiple sclerosis".)
EPIDEMIOLOGY — Most cases of acute demyelinating optic neuritis occur in women (two-thirds) and typically develop in patients between the ages of 20 and 40 [5-7].
The incidence of optic neuritis is highest in populations located at higher latitudes, in the northern United States and western Europe, and is lowest in regions closer to the equator. In the United States, studies have estimated the annual incidence of optic neuritis to be as high as 6.4 per 100,000 [8,9]. In the United States, optic neuritis occurs more frequently in whites than blacks . In Asia, optic neuritis is proportionately more common relative to the incidence of multiple sclerosis than in the United States or Western Europe .
PATHOPHYSIOLOGY — The most common pathologic basis for optic neuritis is inflammatory demyelination of the optic nerve. The pathology is similar to that of acute multiple sclerosis (MS) plaques in the brain, with perivascular cuffing, edema in the myelinated nerve sheaths, and myelin breakdown. Inflammation of the retinal vascular endothelium can precede demyelination and is sometimes visibly manifest as retinal vein sheathing . Myelin loss exceeds axonal loss.
It is believed that the demyelination in optic neuritis is immune-mediated, but the specific mechanism and target antigen(s) are unknown. Systemic T cell activation is identified at symptom onset and precedes changes in the cerebrospinal fluid . Systemic changes also normalize earlier (within two to four weeks) than central changes. T cell activation leads to the release of cytokines and other inflammatory agents. B cell activation against myelin basic protein is not seen in peripheral blood but can be demonstrated in the cerebrospinal fluid of patients with optic neuritis .
As with MS, a genetic susceptibility for optic neuritis is suspected. This is supported by an over-representation of certain human leukocyte antigen (HLA) types among patients with optic neuritis [15,16].
Acute features — Optic neuritis is usually monocular in its clinical presentation. In about 10 percent of cases, symptoms occur in both eyes, either simultaneously or in rapid succession . Bilateral optic neuritis is more common in children younger than 12 to 15 years old and also in Asian and black South African patients [17-22]. Because bilateral symptoms are relatively uncommon, they should suggest an alternative cause of optic neuropathy. However, subclinical visual deficits in acuity, contrast sensitivity, color vision, and visual field in the contralateral eye can often be elicited by detailed visual testing in patients with clinically monocular disease [9,23]. Because these deficits usually resolve along with the clinical deficits in the symptomatic eye, it is unlikely that these findings represent prior episodes of optic neuritis.
Other clinical features of optic neuritis were systematically characterized in the Optic Neuritis Treatment Trial (ONTT), which enrolled 457 patients, aged 18 to 46 years, with acute unilateral optic neuritis [7,24]. The two most common symptoms of optic neuritis are vision loss and eye pain:
●Vision loss typically develops over a period of hours to days, peaking within one to two weeks. Continued deterioration after that time suggests an alternative diagnosis [1,2]. Greater than 90 percent of patients in the ONTT had a significant decrease in central visual acuity. In most, the visual acuities ranged from 20/25 to 20/190 (median visual acuity 20/60). However, some patients had 20/20 acuity (11 percent), and, at the other extreme, a few had no light perception (3 percent).
●Eye pain occurred in 92 percent of patients in the ONTT and often worsened with eye movement . The onset of pain generally coincided with the visual acuity loss and improved along with it.
Other common visual symptoms and signs include:
●An afferent pupillary defect always occurs in optic neuritis if the other eye is uninvolved and otherwise healthy. This is demonstrated by shining a light alternately in one eye and then the other and finding that the direct response to light is more sluggish in the affected eye. The room should be dark, and the patient should fixate on a distant target to prevent miosis due to accommodation. (See "The detailed neurologic examination in adults", section on 'Afferent pupillary defect'.)
●The visual field defect in optic neuritis is typically characterized as a central scotoma [1,25]. However, in the ONTT, almost all types of visual field defects were seen, including diffuse vision loss and altitudinal, arcuate, hemianopic, and cecocentral defects. Nonetheless, a defect that extends to the periphery should suggest a compressive lesion, while an altitudinal defect, particularly an inferior altitudinal defect, is more common in anterior ischemic optic neuropathy [1,25]. Visual field defects usually resolve; in the ONTT, 56 percent had normalized at one year and 73 percent had normalized at 10 years [26,27].
●Papillitis with hyperemia and swelling of the disk, blurring of disk margins, and distended veins is seen in one-third of patients with optic neuritis (picture 1) . Two-thirds of these patients have retrobulbar neuritis with a normal funduscopic examination (picture 2). Papillitis is more common in children less than 14 years old and in certain ethnic populations, including black South Africans and Southeast Asians [11,18-20]. Peripapillary hemorrhages are rare in optic neuritis, but are a common accompaniment to papillitis due to anterior ischemic optic neuropathy .
●Photopsias (flickering or flashes of light) are often precipitated with eye movement and were reported by 30 percent of patients in the ONTT .
●Loss of color of vision out of proportion to the loss of visual acuity is specific to optic nerve pathology. Abnormal color vision by Ishihara plates was found in 88 percent of involved eyes in the ONTT; this increased to 94 percent with the more sensitive Farnsworth-Munsell 100 hue test .
●Other signs of ocular inflammation may be observed by the ophthalmologist on funduscopic or slit lamp examination. Perivenous sheathing or periphlebitis retinae can be seen in about 12 percent of patients with optic neuritis and implies a high risk for multiple sclerosis (MS) [9,12]. Uveitis, cells in the anterior chamber, and/or pars planitis are uncommonly seen in optic neuritis and are more typical of infections and other autoimmune diseases. (See "Optic neuropathies".)
Chronic features — Even after clinical recovery, signs of optic neuritis can persist. These signs in a patient without a history of optic neuritis may suggest a previous, subclinical attack. When a patient presents with a possible first attack of MS elsewhere in the central nervous system, these signs are often sought because evidence of other demyelinating episodes separated in "time and space" can affect prognosis and treatment decisions. (See "Clinically isolated syndromes suggestive of multiple sclerosis".)
Chronic signs of optic neuritis can include:
●Persistent visual loss. Most patients with optic neuritis recover functional vision within one year. However, on testing, deficits in color vision, contrast sensitivity, stereo acuity, and light brightness are detectable in most patients at up to two years . (See "Optic neuritis: Prognosis and treatment", section on 'Recovery of vision'.)
●A relative afferent pupillary defect remains in approximately one-fourth of patients two years after presentation .
●Color desaturation refers to a qualitative inter-eye difference in color perception that can be tested by comparing vision of a red object with each eye. A patient with monocular "red desaturation" may report that the red color appears "washed out," pink, or orange when viewed with the affected eye.
●Temporary exacerbations of visual problems in patients can occur with increased body temperature (Uhthoff's phenomenon). Hot showers and exercise are classic precipitants.
●Optic atrophy to at least some degree almost always follows an attack of optic neuritis, despite the return of visual acuity . Normal, 20/20 visual acuity requires less than one-half of normal foveal axons . The disc appears shrunken and pale, particularly in its temporal half (temporal pallor). The disk pallor extends beyond the margins of the disk into the peripapillary retinal nerve fiber layer.
●The pattern-shift visual evoked response remains delayed in most patients, even with visual recovery. Although latencies continue to shorten (improve) up to two years after presentation, abnormalities are seen in most (80 percent) at two years [28,31,32]. (See 'Visual evoked response' below.)
DIFFERENTIAL DIAGNOSIS — In a young child, infectious and postinfectious causes of optic nerve impairment should be considered as alternatives to optic neuritis, while in an older patient (>50 years), ischemic optic neuropathy (due, for example, to diabetes mellitus or giant cell arteritis) is a more likely diagnosis than optic neuritis.
Alternative diagnoses should also be considered in patients with a bilateral presentation or those with other neurologic or systemic symptoms.
In cases of recurrent optic neuritis that are not due to neuromyelitis optica or MS, other causes of recurrent optic neuritis should be thoroughly investigated (such as sarcoidosis, lupus, chronic relapsing inflammatory optic neuropathy (CRION), or paraneoplastic optic neuropathy (serum CRMP-5/CV2 antibody)).
EVALUATION AND DIAGNOSIS
Diagnosis — In general, optic neuritis is a clinical diagnosis based upon the history and examination findings. Because important findings on funduscopic examination help differentiate typical from atypical cases of optic neuritis, an ophthalmologic examination should be considered an essential feature of the clinical evaluation. Magnetic resonance imaging study of the brain and orbits with gadolinium contrast provides confirmation of the diagnosis in most cases and also provides and assessment of the risk of subsequent multiple sclerosis.
Further diagnostic testing is directed toward excluding other causes of visual loss in atypical cases (See 'Differential diagnosis' above.)
Magnetic resonance imaging — A magnetic resonance imaging study (MRI) of the brain and orbits with gadolinium contrast provides confirmation of the diagnosis of acute demyelinating optic neuritis and important prognostic information regarding the risk of developing MS.
Innovations in MRI technology (eg, short tau inversion recovery [STIR], fast spin echo [FSE], and fluid-attenuated inversion recovery with fat suppression techniques [FLAIR], diffusion tensor imaging [DTI]) have improved imaging of the optic nerve [33-35]. Optic nerve inflammation can be demonstrated in about 95 percent of patients with optic neuritis with gadolinium contrast-enhanced MRI of the brain and orbits (image 1) [6,36-38]. The longitudinal extent of nerve involvement as seen on MRI correlates with visual impairment at presentation and with visual prognosis [31,36,38]. Gadolinium enhancement persists for a mean of 30 days since onset . The signal abnormality in the nerve can still be seen after recovery of vision, and is also present in as many as 60 percent of patients with MS who do not have a clinical history of optic neuritis [31,39-41].
The brain MRI often shows white matter abnormalities characteristic of MS (image 2). Typical lesions are ovoid, periventricular, and larger than 3 mm. (See "Diagnosis of multiple sclerosis in adults", section on 'Lesion characteristics'.) The reported prevalence of white matter abnormalities varies substantially among patients with optic neuritis (23 to 75 percent) . In the ONTT, almost 40 percent of patients had MRI lesions, but this trial represents a selected patient group . Small case series of unselected patients have noted a higher coincidence of MRI brain lesions [31,43,44]. Individuals with white matter abnormalities are at a higher risk of developing MS. (See "Optic neuritis: Prognosis and treatment".)
The yield of spinal cord imaging is low in unselected patients. Among 115 patients presenting with optic neuritis, MRI abnormalities in the spinal cord were seen in only four patients with a normal brain MRI .
Lumbar puncture — Lumbar puncture is not an essential diagnostic test in optic neuritis, but should be considered in atypical cases (eg, those with bilateral presentation, <15 years in age, or symptoms suggesting infection) [45,46]. (See "Optic neuropathies", section on 'Infections'.)
Approximately 60 to 80 percent of patients with acute optic neuritis have nonspecific abnormalities in the cerebrospinal fluid (CSF), including lymphocytes (10 to 100) and elevated protein .
Other CSF findings in optic neuritis can include :
●Myelin basic protein in about 20 percent
●IgG synthesis in 20 to 36 percent
●Oligoclonal bands (OCB) in 56 to 69 percent
The presence of OCB implies a higher risk of developing MS. However, since OCB are also associated with white matter lesions on brain MRI, their presence is not clearly of independent prognostic importance . (See "Optic neuritis: Prognosis and treatment".)
Other testing — When there are relevant clues to an alternative diagnosis (table 2), measurement of the erythrocyte sedimentation rate, antinuclear antibodies, and angiotensin converting enzyme levels and serologic and CSF tests for Lyme disease and syphilis should be obtained [45,46]. (See "Optic neuropathies".)
Fluorescein angiography — Fluorescein angiography is not routinely performed in the evaluation of optic neuritis and is often normal. Up to 25 percent demonstrate either dye leakage or perivenous sheathing . These findings may identify patients at somewhat higher risk for developing MS.
Visual evoked response — A delay in the P100 of the visual evoked response (VER) is the electrophysiologic manifestation of slowed conduction in the optic nerve as a result of axonal demyelination . This test is not usually helpful in the diagnosis of acute optic neuritis, unless there is a suspicion that the visual loss is functional.
Abnormalities in the VER can persist after recovery of full vision. At one year, 80 to 90 percent will be abnormal; 35 percent will return to normal at two years [28,31,32]. The VER is often employed to find evidence of previous, asymptomatic, episodes of optic neuritis, but the sensitivity and specificity are imperfect .
The multifocal VER is a technical advance that appears to be more sensitive and specific for identifying optic neuritis, but this technology is not generally available [1,49].
Optical coherence tomography — Optical coherence tomography (OCT) measures the thickness in the retinal nerve fiber layer and detects thinning in most (85 percent) of patients with optic neuritis [48,50-53]. These abnormalities are also common in patients with MS who do not have a clinical history of optic neuritis . While lower values correlate with impaired visual outcome, the utility of OCT as a prognostic tool is limited in that abnormal values do not show up until early swelling disappears. In one study, OCT was less sensitive than VER in detecting subclinical optic neuritis .
A number of studies have found that a greater severity of optic nerve injury seen on OCT suggests neuromyelitis optica rather than optic neuritis associated with multiple sclerosis [56-58].
Aquaporin-4-specific serum autoantibody — Patients with recurrent optic neuritis may be particularly at risk neuromyelitis optica (NMO) or Devic's disease. This is particularly true for patients with a normal brain MRI and those with optic neuritis events in rapid succession or with a presentation of severe vision loss . In one series of 51 patients with either severe or recurrent optic neuritis, six patients were seropositive for the aquaporin-4-specific serum autoantibody, a sensitive biomarker for NMO while 10 patients were seropositive for antibodies to myelin-oligodendrocyte glycoprotein (MOG), which has also been associated with NMO . In other studies, seropositivity for the aquaporin-4-specific serum autoantibody was predictive of subsequent NMO among patients with recurrent optic neuritis [61,62]. The serum NMO antibody test is suggested for individuals with recurrent ON, particularly if the MRI brain is negative for any abnormal T2/FLAIR lesions outside of the affected optic nerve(s). The role for testing MOG antibodies is investigational .
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
●Basics topic (see "Patient education: Optic neuritis (The Basics)")
SUMMARY AND RECOMMENDATIONS — Optic neuritis is an acute inflammatory demyelinating injury to the optic nerve.
●In typical cases, painful, monocular visual loss evolves over several hours to a few days. One-third of patients have visible optic nerve inflammation on funduscopic examination (papillitis); in the remainder, the inflammation is retrobulbar. (See 'Acute features' above.)
●Chronic signs of optic neuritis include a relative afferent pupillary defect, color desaturation, and optic atrophy. These often persist despite recovery of normal vision. (See 'Chronic features' above.)
●A gadolinium-enhanced MRI of the brain and orbits provides confirmation of optic neuritis and aids in the assessment of prognosis and treatment decisions. Other tests, including lumbar puncture, fluorescein angiography, and visual evoked potentials are used in atypical cases. (See 'Evaluation and diagnosis' above.)
- Balcer LJ. Clinical practice. Optic neuritis. N Engl J Med 2006; 354:1273.
- Foroozan R, Buono LM, Savino PJ, Sergott RC. Acute demyelinating optic neuritis. Curr Opin Ophthalmol 2002; 13:375.
- Frohman EM, Frohman TC, Zee DS, et al. The neuro-ophthalmology of multiple sclerosis. Lancet Neurol 2005; 4:111.
- Arnold AC. Evolving management of optic neuritis and multiple sclerosis. Am J Ophthalmol 2005; 139:1101.
- Liu GT. Visual loss: optic neuropathies. In: Neuro-Ophthalmology: Diagnosis and Management, Liu GT, Volpe NJ, Galetta SL (Eds), WB Saunders, Philadelphia 2001.
- Wray SH. Optic neuritis.. In: Principles and Practice of Ophthalmology, Albert DM, Jakobiec FA (Eds), WB Saunders, Philadelphia 1994. p.2539.
- The clinical profile of optic neuritis. Experience of the Optic Neuritis Treatment Trial. Optic Neuritis Study Group. Arch Ophthalmol 1991; 109:1673.
- Percy AK, Nobrega FT, Kurland LT. Optic neuritis and multiple sclerosis. An epidemiologic study. Arch Ophthalmol 1972; 87:135.
- Rodriguez M, Siva A, Cross SA, et al. Optic neuritis: a population-based study in Olmsted County, Minnesota. Neurology 1995; 45:244.
- Phillips PH, Newman NJ, Lynn MJ. Optic neuritis in African Americans. Arch Neurol 1998; 55:186.
- Wakakura M, Minei-Higa R, Oono S, et al. Baseline features of idiopathic optic neuritis as determined by a multicenter treatment trial in Japan. Optic Neuritis Treatment Trial Multicenter Cooperative Research Group (ONMRG). Jpn J Ophthalmol 1999; 43:127.
- Lightman S, McDonald WI, Bird AC, et al. Retinal venous sheathing in optic neuritis. Its significance for the pathogenesis of multiple sclerosis. Brain 1987; 110 ( Pt 2):405.
- Roed H, Frederiksen J, Langkilde A, et al. Systemic T-cell activation in acute clinically isolated optic neuritis. J Neuroimmunol 2005; 162:165.
- Söderström M, Link H, Xu Z, Fredriksson S. Optic neuritis and multiple sclerosis: anti-MBP and anti-MBP peptide antibody-secreting cells are accumulated in CSF. Neurology 1993; 43:1215.
- Frederiksen JL, Madsen HO, Ryder LP, et al. HLA typing in acute optic neuritis. Relation to multiple sclerosis and magnetic resonance imaging findings. Arch Neurol 1997; 54:76.
- Francis DA, Compston DA, Batchelor JR, McDonald WI. A reassessment of the risk of multiple sclerosis developing in patients with optic neuritis after extended follow-up. J Neurol Neurosurg Psychiatry 1987; 50:758.
- de la Cruz J, Kupersmith MJ. Clinical profile of simultaneous bilateral optic neuritis in adults. Br J Ophthalmol 2006; 90:551.
- Pokroy R, Modi G, Saffer D. Optic neuritis in an urban black African community. Eye (Lond) 2001; 15:469.
- Hwang JM, Lee YJ, Kim MK. Optic neuritis in Asian children. J Pediatr Ophthalmol Strabismus 2002; 39:26.
- Wang JC, Tow S, Aung T, et al. The presentation, aetiology, management and outcome of optic neuritis in an Asian population. Clin Exp Ophthalmol 2001; 29:312.
- Lucchinetti CF, Kiers L, O'Duffy A, et al. Risk factors for developing multiple sclerosis after childhood optic neuritis. Neurology 1997; 49:1413.
- Wilejto M, Shroff M, Buncic JR, et al. The clinical features, MRI findings, and outcome of optic neuritis in children. Neurology 2006; 67:258.
- Beck RW, Kupersmith MJ, Cleary PA, Katz B. Fellow eye abnormalities in acute unilateral optic neuritis. Experience of the optic neuritis treatment trial. Ophthalmology 1993; 100:691.
- Beck RW. The Optic Neuritis Treatment Trial. Arch Ophthalmol 1988; 106:1051.
- Gerling J, Meyer JH, Kommerell G. Visual field defects in optic neuritis and anterior ischemic optic neuropathy: distinctive features. Graefes Arch Clin Exp Ophthalmol 1998; 236:188.
- Keltner JL, Johnson CA, Spurr JO, Beck RW. Visual field profile of optic neuritis. One-year follow-up in the Optic Neuritis Treatment Trial. Arch Ophthalmol 1994; 112:946.
- Beck RW, Gal RL, Bhatti MT, et al. Visual function more than 10 years after optic neuritis: experience of the optic neuritis treatment trial. Am J Ophthalmol 2004; 137:77.
- Brusa A, Jones SJ, Plant GT. Long-term remyelination after optic neuritis: A 2-year visual evoked potential and psychophysical serial study. Brain 2001; 124:468.
- Cleary PA, Beck RW, Bourque LB, et al. Visual symptoms after optic neuritis. Results from the Optic Neuritis Treatment Trial. J Neuroophthalmol 1997; 17:18.
- Miller NR, Newman NJ, Biousse V, Kerrison JB. Walsh and Hoyt's Clinical Neuro-ophthalmology, Lippincott, Williams and Wilkins, Philadelphia 2005.
- Hickman SJ, Toosy AT, Miszkiel KA, et al. Visual recovery following acute optic neuritis--a clinical, electrophysiological and magnetic resonance imaging study. J Neurol 2004; 251:996.
- Celesia GG, Kaufman DI, Brigell M, et al. Optic neuritis: a prospective study. Neurology 1990; 40:919.
- Barker GJ. Technical issues for the study of the optic nerve with MRI. J Neurol Sci 2000; 172 Suppl 1:S13.
- Jackson A, Sheppard S, Laitt RD, et al. Optic neuritis: MR imaging with combined fat- and water-suppression techniques. Radiology 1998; 206:57.
- Naismith RT, Xu J, Tutlam NT, et al. Disability in optic neuritis correlates with diffusion tensor-derived directional diffusivities. Neurology 2009; 72:589.
- Rizzo JF 3rd, Andreoli CM, Rabinov JD. Use of magnetic resonance imaging to differentiate optic neuritis and nonarteritic anterior ischemic optic neuropathy. Ophthalmology 2002; 109:1679.
- Rocca MA, Hickman SJ, Bö L, et al. Imaging the optic nerve in multiple sclerosis. Mult Scler 2005; 11:537.
- Kupersmith MJ, Alban T, Zeiffer B, Lefton D. Contrast-enhanced MRI in acute optic neuritis: relationship to visual performance. Brain 2002; 125:812.
- Youl BD, Turano G, Towell AD, et al. Optic neuritis: swelling and atrophy. Electroencephalogr Clin Neurophysiol Suppl 1996; 46:173.
- Miller DH, Newton MR, van der Poel JC, et al. Magnetic resonance imaging of the optic nerve in optic neuritis. Neurology 1988; 38:175.
- Davies MB, Williams R, Haq N, et al. MRI of optic nerve and postchiasmal visual pathways and visual evoked potentials in secondary progressive multiple sclerosis. Neuroradiology 1998; 40:765.
- Dalton CM, Brex PA, Miszkiel KA, et al. Spinal cord MRI in clinically isolated optic neuritis. J Neurol Neurosurg Psychiatry 2003; 74:1577.
- Jacobs LD, Kaba SE, Miller CM, et al. Correlation of clinical, magnetic resonance imaging, and cerebrospinal fluid findings in optic neuritis. Ann Neurol 1997; 41:392.
- Städt D, Kappos L, Rohrbach E, et al. Occurrence of MRI abnormalities in patients with isolated optic neuritis. Eur Neurol 1990; 30:305.
- Boomer JA, Siatkowski RM. Optic neuritis in adults and children. Semin Ophthalmol 2003; 18:174.
- Beck RW, Trobe JD. What we have learned from the Optic Neuritis Treatment Trial. Ophthalmology 1995; 102:1504.
- Nilsson P, Larsson EM, Maly-Sundgren P, et al. Predicting the outcome of optic neuritis: evaluation of risk factors after 30 years of follow-up. J Neurol 2005; 252:396.
- Klistorner A, Arvind H, Nguyen T, et al. Axonal loss and myelin in early ON loss in postacute optic neuritis. Ann Neurol 2008; 64:325.
- Fraser CL, Klistorner A, Graham SL, et al. Multifocal visual evoked potential analysis of inflammatory or demyelinating optic neuritis. Ophthalmology 2006; 113:323.e1.
- Costello F, Coupland S, Hodge W, et al. Quantifying axonal loss after optic neuritis with optical coherence tomography. Ann Neurol 2006; 59:963.
- Trip SA, Schlottmann PG, Jones SJ, et al. Retinal nerve fiber layer axonal loss and visual dysfunction in optic neuritis. Ann Neurol 2005; 58:383.
- Fisher JB, Jacobs DA, Markowitz CE, et al. Relation of visual function to retinal nerve fiber layer thickness in multiple sclerosis. Ophthalmology 2006; 113:324.
- de Seze J, Blanc F, Jeanjean L, et al. Optical coherence tomography in neuromyelitis optica. Arch Neurol 2008; 65:920.
- Yeh EA, Marrie RA, Reginald YA, et al. Functional-structural correlations in the afferent visual pathway in pediatric demyelination. Neurology 2014; 83:2147.
- Naismith RT, Tutlam NT, Xu J, et al. Optical coherence tomography is less sensitive than visual evoked potentials in optic neuritis. Neurology 2009; 73:46.
- Naismith RT, Tutlam NT, Xu J, et al. Optical coherence tomography differs in neuromyelitis optica compared with multiple sclerosis. Neurology 2009; 72:1077.
- Ratchford JN, Quigg ME, Conger A, et al. Optical coherence tomography helps differentiate neuromyelitis optica and MS optic neuropathies. Neurology 2009; 73:302.
- Green AJ, Cree BA. Distinctive retinal nerve fibre layer and vascular changes in neuromyelitis optica following optic neuritis. J Neurol Neurosurg Psychiatry 2009; 80:1002.
- Pirko I, Blauwet LA, Lesnick TG, Weinshenker BG. The natural history of recurrent optic neuritis. Arch Neurol 2004; 61:1401.
- Martinez-Hernandez E, Sepulveda M, Rostásy K, et al. Antibodies to aquaporin 4, myelin-oligodendrocyte glycoprotein, and the glycine receptor α1 subunit in patients with isolated optic neuritis. JAMA Neurol 2015; 72:187.
- Matiello M, Lennon VA, Jacob A, et al. NMO-IgG predicts the outcome of recurrent optic neuritis. Neurology 2008; 70:2197.
- Takagi M, Tanaka K, Suzuki T, et al. Anti-aquaporin-4 antibody-positive optic neuritis. Acta Ophthalmol 2009; 87:562.
- Petzold A, Pittock S, Lennon V, et al. Neuromyelitis optica-IgG (aquaporin-4) autoantibodies in immune mediated optic neuritis. J Neurol Neurosurg Psychiatry 2010; 81:109.