eMedicine Specialties > Radiology > Head/Neck

Optic Neuritis

Author: Pil (Peter) S Kang, MD,, Attending Radiologist, Diagnostic Radiology, Department of Diagnostic Radiology, Walter Reed Army Medical Center; Associate Professor, Department of Radiology, Uniformed Services University of Health Sciences
Coauthor(s): Fletcher M Munter, MD, Program Director, National Capital Consortium Radiology Residency; Consulting Staff, Department of Radiology, Walter Reed Army Medical Center; Charles Swallow, MD, Department of Radiology, St Marks Hospital
Contributor Information and Disclosures

Updated: Jun 23, 2009

Introduction

Background

Optic neuritis is defined as inflammation of the optic nerve. It is one of the causes of acute loss of vision associated with pain. Optic neuritis can be the initial episode for a patient who will subsequently develop multiple sclerosis.

A 43-year-old woman with acute vision loss and ey...

A 43-year-old woman with acute vision loss and eye pain. No prior neurologic symptoms were noted. Axial short tau inversion recovery image demonstrates faint increased signal in the distal left optic nerve.

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A 43-year-old woman with acute vision loss and ey...

A 43-year-old woman with acute vision loss and eye pain. No prior neurologic symptoms were noted. Axial short tau inversion recovery image demonstrates faint increased signal in the distal left optic nerve.



A 35-year-old woman with acute onset of left eye ...

A 35-year-old woman with acute onset of left eye pain and vision decline. Axial fat-suppressed postcontrast T1-weighted image demonstrates enhancement in the intracanalicular portion of the left optic nerve.

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A 35-year-old woman with acute onset of left eye ...

A 35-year-old woman with acute onset of left eye pain and vision decline. Axial fat-suppressed postcontrast T1-weighted image demonstrates enhancement in the intracanalicular portion of the left optic nerve.



The diagnosis of optic neuritis is usually made clinically. Although direct imaging of the optic nerves by MRI is reserved for atypical cases, MRI of the brain yields information that can change management and yield prognostic information in terms of the patient's future risk for development of multiple sclerosis. As established by the Optic Neuritis Treatment Trial, an abnormal baseline brain MRI is a strong predictor of MS after isolated optic neuritis in adults.1,2,3  

Bonhomme et al studied the rate of conversion to multiple sclerosis (MS) after a diagnosis of optic neuritis in children (younger than 18 y) who presented with optic neuritis between 1993 and 2004 at the Children's Hospital of Philadelphia. They found that children with brain MRI abnormalities at the time of optic neuritis diagnosis had an increased risk for MS. In the study, they identified 29 children with idiopathic optic neuritis. Eleven of the 29 patients (38%) had white-matter T2/FLAIR lesions in the brain (not including the optic nerves). Eighteen patients were followed for more than 24 months, and 3 of the 18 (17%) developed MS. All 3 patients who developed MS had an abnormal brain MRI scan at their initial presentation of optic neuritis. None of the patients who had normal MRI scans developed MS over an average follow-up of 88.5 months.1

Swanton et al investigated patients with optic neuritis to determine the influence of lesion number, location and activity, and non-lesion MRI measures obtained on early scans. At 6-year follow-up, 48% of patients had converted to clinically definite MS, and 52% remained with clinically isolated syndrome. The presence and the number of spinal cord lesions at baseline and new T2 lesions at follow-up were found to be significant independent predictors of higher disability. Disability was also predicted by the presence at baseline of gadolinium-enhancing lesions and the number of infratentorial lesions. Only spinal cord lesions predicted disability in patients converting to clinically definite MS.4

Patients in the Optic Neuritis Treatment Trial, who were enrolled between July 1, 1988, and June 30, 1991,3 were followed up prospectively for 15 years, with the final examination of 389 patients with acute optic neuritis occurring in 2006 to determine development of MS and neurologic disability. The cumulative probability of developing MS by 15 years after onset of optic neuritis was 50% and was strongly related to the presence of lesions on a baseline non-contrast-enhanced MRI of the brain. Twenty-five percent of patients with no lesions on baseline brain MRI developed MS during follow-up, compared with 72% of patients with 1 or more lesions.2

Pathophysiology

The inflammation of the optic nerve is mainly due to demyelination and can be idiopathic and isolated. However, this disease has a very strong association with multiple sclerosis.5,6 From 15 to 20% of cases of multiple sclerosis manifest as optic neuritis, and 38-50% of patients with multiple sclerosis develop optic neuritis at some point during the course of their disease. According to one of the more well-known long-term, follow-up series of optic neuritis, the risk of development of multiple sclerosis after an episode of isolated optic neuritis was 30% at 5-year follow-up and 38% at 10-year follow-up.

Neuromyelitis optica, also known as Devic disease, is a rare demyelinating process that affects the optic nerve.7,8,9,10 This disease is frequently misdiagnosed as multiple sclerosis, but it is a separate entity that is distinguished from multiple sclerosis by its severity, by disease location (affects the optic nerves and the spinal cord, sparing the brain), and by cerebrospinal fluid analysis (polymorphonuclear pleocytosis and absence of oligoclonal banding).

Although demyelination is the most common identifiable cause of optic neuritis, other causes of optic nerve inflammation include Lyme disease, tuberculosis, syphilis, and viral agents such as HIV, hepatitis B virus, herpes virus, and cytomegalovirus. Secondary involvement from paranasal sinus infection and orbital cysticercosis has been described. Optic neuritis also may occur as a complication of radiation therapy. Much rarer causes, such as drugs (concurrent etanercept and isoniazid therapy, ethambutol in the setting of end-stage renal disease, interferon alfa), gluten sensitivity, hypereosinophilic syndrome, and vasculitis (giant cell arteritis),11 have been reported in the literature as case reports.

Lesions of the optic nerve in idiopathic and multiple sclerosis–related optic neuritis are similar to the plaques seen in multiple sclerosis of the brain. In acute optic neuritis, lesions are sharply defined areas of myelin sheath loss with relative preservation of the axons. Large numbers of foamy macrophages are present, along with cholesterol ester droplets and abundant lymphocyte and plasma cell accumulations.

In later stages of the disease, the numbers of lymphocytes, plasma cells, and macrophages diminish and astrocytic scar formation occurs. Little remyelination of the damaged axons in lesions is associated with chronic multiple sclerosis, but evidence of oligodendrocyte precursor cells and remyelination attempts in early multiple sclerosis and acute lesions has been documented. This suggests that potential therapeutic interventions that promote myelin formation may play a role in improved recovery.

The lack of remyelination in chronic lesions often is manifested clinically by abnormal visual-evoked potentials, even when Snellen chart visual acuity has returned to normal or near normal in most patients. Functional MRI studies have demonstrated extra-occipital sites of activation during visual stimuli, particularly involving the insula, claustrum, lateral temporal lobe, thalamus, and posterior parietal and orbitofrontal regions. This suggests that a functional reorganization of cerebral responses to abnormal or delayed stimuli from the damaged nerves may occur as an adaptive mechanism. Long-term visual-evoked potential studies suggest that some degree of partial remyelination or ion channel reorganization in the optic nerves may occur up to 2 years after the initial demyelination event. However, this may be counterbalanced by recurrent subclinical episodes of demyelination.

Various genetic and environmental factors are presumed to predispose patients to demyelination as an autoimmune response. The presence of alleles for HLA-Dw2 or HLA-DR2 is a known risk factor in the development of multiple sclerosis and optic neuritis. However, in a Swedish cohort, the allele for HLA-Dw2 was present in only 47% of affected patients. Viral or bacterial infection, stress, and systemic antigens and metabolites have been proposed as possible initiating events that result in autoreactive antibodies and T cells crossing the blood-brain barrier and injuring myelin.12

Anatomy

MRI studies have been performed to identify the most common sites of optic nerve involvement in optic neuritis. The nerve can be divided into 5 segments (each with frequency of involvement), including (1) anterior (45%), abutting the optic disc; (2) mid intraorbital (61%); (3) intracanalicular (34%); (4) intracranial prechiasmatic (5%); and (5) chiasmatic segments (2%). Lesions occasionally involve more than one site.

Presentation

The classic triad of optic neuritis consists of (1) loss of vision, (2) eye pain, and (3) dyschromatopsia, which refers to the impairment of accurate color vision. Seventy percent of cases in adults are unilateral. The typical clinical course is that of eye pain and worsening visual function, which progresses over days to weeks. The eye pain usually resolves over days, often as the visual loss begins. The patients usually recover spontaneously, with recovery of visual loss beginning within 2-3 weeks and stabilizing over months.

Additional associated clinical findings may include movement- or sound-induced phosphenes, described as brief flashes of light lasting 1-2 seconds. Reduction in vision may worsen in bright light, a symptom that seems paradoxical. The Uhthoff symptom, described as exercise- or heat-induced vision loss, may occur and has been described in 50% of patients with isolated optic neuritis. Physical examination findings may include an afferent pupillary defect and a swollen optic disc.

Whites of northern European descent are affected 8 times more frequently than blacks and Asians. Whites of Mediterranean ancestry are at intermediate risk. African blacks and Asians are rarely affected. In the United States, the male-to-female ratio for optic neuritis is 1:1.8. The mean age of onset is approximately 30 years, with most patients presenting from age 20-40 years.

The condition is rare in children and is usually related to a postinfectious or parainfectious demyelination.13 Optic neuritis in children is less likely to progress to multiple sclerosis, but, in some reports, it has a worse prognosis for full vision recovery. In patients older than age 50 years, optic neuritis is less common and may be mistaken for ischemic optic neuropathy, which is more common in persons in this age group.

Irreversible optic nerve damage occurs in up to 85% of patients; however, this damage often is subclinical. As many as 80% of patients regain at least 20/30 vision, 45% within the first 4 months and 35% within 1 year. Long-term severe vision loss occurs in 20% of patients. This morbidity is separate from that associated with multiple sclerosis.

Occasionally, subclinical optic neuritis is discovered in patients during an evaluation for demyelination suspected for other reasons. These subclinical cases may be detected electrophysiologically by visual-evoked potentials or by careful physical examination if dyschromatopsia, optic disc pallor, and characteristic nerve fiber layer slits are discovered.

The demographics of incidence and prevalence rates of optic neuritis in the United States closely follow those of multiple sclerosis; therefore, the prevalence of optic neuritis is highest among white populations of northern European ancestry, is moderately high in white populations of Mediterranean ancestry, and is low in African black or Asian populations. In the United States, the annual incidence in a predominantly white community is 6.4 cases per 100,000 persons.

Optic neuritis not uncommonly recurs, either in the same or the contralateral eye. The Optic Neuritis Treatment Trial showed that 28% and 35% of patients developed recurrence within 5 and 10 years, respectively. Not surprisingly, recurrence was more common in patients who were subsequently diagnosed with multiple sclerosis. The cumulative probability of developing MS by 15 years after onset of optic neuritis was 50% and was strongly related to the presence of lesions on a baseline non-contrast-enhanced MRI of the brain. Twenty-five percent of patients with no lesions on baseline brain MRI developed MS during follow-up, compared with 72% of patients with 1 or more lesions.2,14

Most persons with optic neuritis recover spontaneously. Intravenous methylprednisolone therapy has been shown to increase rates of visual recovery but without significant long-term benefit for visual function. Corticosteroids, therefore, are considered for patients who require faster recovery, such as monocular patients, patients with severe bilateral visual loss, or those with occupations requiring high level of visual acuity.

Treatment with corticosteroids and/or immunomodulation agents (eg, interferon beta-1a, interferon beta-1b, glatiramer acetate) can be considered in patients who are at higher risk of developing multiple sclerosis. This is determined predominantly by MRI of the brain.

Preferred Examination

The diagnosis of optic neuritis is usually made on clinical grounds, supplemented by ophthalmologic examination findings. However, in atypical cases (eg, prolonged or severe pain, lack of visual recovery, atypical visual-field loss, evidence of orbital inflammation and/or inflammation), MRI is used to further characterize and to exclude other disease processes.

Thin (2-3 mm) fat-suppressed T2-weighted images, such as short tau inversion recovery sequences, through the optic nerves may show characteristic high-signal intensity foci in the minimally or nonexpanded nerve. These lesions frequently enhance following intravenous contrast administration, which is not seen in a healthy optic nerve. Some studies have shown that certain findings, such as optic nerve lesions of greater length and in certain locations (within optic canal), might be associated with a worse visual prognosis and might benefit from certain treatments, but other studies have not supported this conclusion.

Diffusion-weighted and diffusion-tensor imaging may contribute more data that may prove to have some bearing on treatment and/or on prognosis. The thought is that the loss of anisotropy (manifested by an increase in the apparent diffusion coefficient or decrease in fractional anisotropy) associated with demyelination and/or axonal damage may be more sensitive and/or yield more prognostic information than anatomic imaging findings (size, T2 signal intensity, and enhancement, which suggests loss of the blood-brain barrier due to the underlying pathologic process), which could manifest themselves much later than the findings associated with loss of anisotropy. However, with the current technology, diffusion-weighted and diffusion-tensor imaging of the optic nerves is too time- and labor-intensive for broad clinical application.

The real contribution of imaging in the setting of optic neuritis is made by imaging the brain, not the optic nerves themselves. This is due to the fact that the most valuable predictor for the development of subsequent multiple sclerosis is the presence of white-matter abnormalities. From 27 to 70% (in various studies) of patients with isolated optic neuritis show abnormal MRI findings of the brain, as defined by 2 or more white-matter lesions on T2-weighted images. In the Optic Nerve Treatment Trial, the 5-year risk of developing multiple sclerosis was 16% in patients with normal brain MRI findings, 37% with 1-2 lesions, and 51% with 3 or more lesions. At 10 years, the only statistically significant difference was between no lesions (22% risk) and one or more lesions (56% risk).14

In addition, information from brain MRI has a potential influence on treatment. It has been shown that in 2-year follow-up of patients with optic neuritis and 2 or more brain lesions on MRIs, patients given intravenous methylprednisolone (as compared with placebo and oral prednisone groups) had a significantly decreased risk of developing multiple sclerosis. Note that this benefit was not maintained at 3 years. In a study using interferon beta-1a (Avonex) in patients with optic neuritis with 2 or more white-matter lesions on MRIs of the brain, a decreased risk of developing multiple sclerosis at 3 years was demonstrated. In those patients who did ultimately develop multiple sclerosis, interferon beta-1a was shown to reduce the disease burden and number of active lesions.

CT scanning has a very limited role in the setting of optic neuritis. Size differences in the optic nerve can be appreciated, but this is neither sensitive nor specific. Contrast-enhanced CT scanning of the orbits may be able to help exclude other orbital pathology, albeit in a limited way relative to MRI, because of the inherently superior soft-tissue contrast resolution yielded with MRI. Certainly, CT scanning of the brain, regardless of whether intravenous contrast material is administered or not, does not yield prognostic and treatment-altering information as does MRI of the brain.

Differential Diagnoses

Brain, Multiple Sclerosis
Orbit, Infection
Sinusitis
Tuberculosis, CNS

Other Problems to Be Considered

Ischemic optic neuropathy
Factitious vision loss
Lyme disease
Compressive optic neuropathy

More on Optic Neuritis

Overview: Optic Neuritis
Imaging: Optic Neuritis
Follow-up: Optic Neuritis
Multimedia: Optic Neuritis
References
Further Reading
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References

  1. Bonhomme GR, Waldman AT, Balcer LJ, Daniels AB, Tennekoon GI, Forman S, et al. Pediatric optic neuritis: brain MRI abnormalities and risk of multiple sclerosis. Neurology. Mar 10 2009;72(10):881-5. [Medline].

  2. Multiple sclerosis risk after optic neuritis: final optic neuritis treatment trial follow-up. Arch Neurol. Jun 2008;65(6):727-32. [Medline].

  3. 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. Jan 2004;137(1):77-83. [Medline].

  4. Swanton JK, Fernando KT, Dalton CM, Miszkiel KA, Altmann DR, Plant GT, et al. Early MRI in optic neuritis: the risk for disability. Neurology. Feb 10 2009;72(6):542-50. [Medline].

  5. Kolappan M, Henderson AP, Jenkins TM, Wheeler-Kingshott CA, Plant GT, Thompson AJ, et al. Assessing structure and function of the afferent visual pathway in multiple sclerosis and associated optic neuritis. J Neurol. Mar 18 2009;[Medline].

  6. Osborne BJ, Volpe NJ. Optic neuritis and risk of MS: differential diagnosis and management. Cleve Clin J Med. Mar 2009;76(3):181-90. [Medline].

  7. Naismith RT, Tutlam NT, Xu J, Klawiter EC, Shepherd J, Trinkaus K, et al. Optical coherence tomography differs in neuromyelitis optica compared with multiple sclerosis. Neurology. Mar 24 2009;72(12):1077-82. [Medline].

  8. Lopategui Cabezas I, Cervantes Llano M, Pentón Rol G. [Optic neuromyelitis: Main differences with multiple sclerosis.]. An Med Interna. Jun 2008;25(6):294-6. [Medline].

  9. Trautner S, Pedersen H, Bendtson I. [Neuromyelitis optica with atypical cerebral lesions demonstrated by magnetic resonance imaging in a 9-year old girl]. Ugeskr Laeger. Jan 26 2009;171(5):334-6. [Medline].

  10. Wingerchuk DM, Weinshenker BG. Neuromyelitis Optica. Curr Treat Options Neurol. May 2005;7(3):173-182. [Medline].

  11. Garcia-Porrua C, Santamarina R, Armesto V, Gonzalez-Gay MA. Magnetic resonance imaging in optic neuritis due to giant cell arteritis. Arthritis Rheum. Apr 15 2005;53(2):313-4. [Medline].

  12. Hauser SL, Oksenberg JR, Lincoln R, et al. Interaction between HLA-DR2 and abnormal brain MRI in optic neuritis and early MS. Optic Neuritis Study Group. Neurology. May 9 2000;54(9):1859-61. [Medline].

  13. Morales DS, Siatkowski RM, Howard CW, Warman R. Optic neuritis in children. J Pediatr Ophthalmol Strabismus. Sep-Oct 2000;37(5):254-9. [Medline].

  14. Optic Neuritis Study Group. Visual function 5 years after optic neuritis: experience of the Optic Neuritis Treatment Trial. The Optic Neuritis Study Group. Arch Ophthalmol. Dec 1997;115(12):1545-52. [Medline].

  15. Wray SH. Optic neuritis. In: Albert DM, Jakobiec FA, eds. Principles and Practice of Ophthalmology. Philadelphia, Pa: WB Saunders; 1994:. 2539-68.

  16. Arnold AC. Evolving management of optic neuritis and multiple sclerosis. Am J Ophthalmol. Jun 2005;139(6):1101-8. [Medline].

  17. Beck RW, Arrington J, Murtagh FR, et al. Brain magnetic resonance imaging in acute optic neuritis. Experience of the Optic Neuritis Study Group. Arch Neurol. Aug 1993;50(8):841-6. [Medline].

  18. Beck RW, Cleary PA, Anderson MM, et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. N Engl J Med. Feb 27 1992;326(9):581-8. [Medline].

  19. Beck RW, Cleary PA, Backlund JC. The course of visual recovery after optic neuritis. Experience of the Optic Neuritis Treatment Trial. Ophthalmology. Nov 1994;101(11):1771-8. [Medline].

  20. Beck RW, Cleary PA, Trobe JD, et al. The effect of corticosteroids for acute optic neuritis on the subsequent development of multiple sclerosis. The Optic Neuritis Study Group. N Engl J Med. Dec 9 1993;329(24):1764-9. [Medline].

  21. Brusa A, Jones SJ, Plant GT. Long-term remyelination after optic neuritis: A 2-year visual evoked potential and psychophysical serial study. Brain. Mar 2001;124(Pt 3):468-79. [Medline].

  22. Brusaferri F, Candelise L. Steroids for multiple sclerosis and optic neuritis: a meta-analysis of randomized controlled clinical trials. J Neurol. Jun 2000;247(6):435-42. [Medline].

  23. Chabert S, Molko N, Cointepas Y, et al. Diffusion tensor imaging of the human optic nerve using a non-CPMG fast spin echo sequence. J Magn Reson Imaging. Aug 2005;22(2):307-10. [Medline].

  24. CHAMPS Study Group. Interferon beta-1a for optic neuritis patients at high risk for multiple sclerosis. Am J Ophthalmol. Oct 2001;132(4):463-71. [Medline].

  25. Ergene E, Rupp FW Jr, Qualls CR, Ford CC. Acute optic neuritis: association with paranasal sinus inflammatory changes on magnetic resonance imaging. J Neuroimaging. Oct 2000;10(4):209-15. [Medline].

  26. Fang JT, Chen YC, Chang MY. Ethambutol-induced optic neuritis in patients with end stage renal disease on hemodialysis: two case reports and literature review. Ren Fail. Mar 2004;26(2):189-93. [Medline].

  27. Ghezzi A, Martinelli V, Rodegher M, et al. The prognosis of idiopathic optic neuritis. Neurol Sci. 2000;21(4 Suppl 2):S865-9. [Medline].

  28. Hickman SJ, Wheeler-Kingshott CA, Jones SJ, et al. Optic nerve diffusion measurement from diffusion-weighted imaging in optic neuritis. AJNR Am J Neuroradiol. Apr 2005;26(4):951-6. [Medline].

  29. Jacob S, Zarei M, Kenton A, Allroggen H. Gluten sensitivity and neuromyelitis optica: two case reports. J Neurol Neurosurg Psychiatry. Jul 2005;76(7):1028-30. [Medline].

  30. Jacobs LD, Beck RW, Simon JH, et al. Intramuscular interferon beta-1a therapy initiated during a first demyelinating event in multiple sclerosis. CHAMPS Study Group. N Engl J Med. Sep 28 2000;343(13):898-904. [Medline].

  31. Kaufman DI, Trobe JD, Eggenberger ER, Whitaker JN. Practice parameter: the role of corticosteroids in the management of acute monosymptomatic optic neuritis. Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. Jun 13 2000;54(11):2039-44. [Medline].

  32. Lee AG, Lin DJ, Kaufman M, et al. Atypical features prompting neuroimaging in acute optic neuropathy in adults. Can J Ophthalmol. Oct 2000;35(6):325-30. [Medline].

  33. Lincoff NS, Schlesinger D. Recurrent optic neuritis as the presenting manifestation of primary hypereosinophilic syndrome: a report of two cases. J Neuroophthalmol. Jun 2005;25(2):116-21. [Medline].

  34. Matsuo T, Takabatake R. Multiple sclerosis-like disease secondary to alpha interferon. Ocul Immunol Inflamm. Dec 2002;10(4):299-304. [Medline].

  35. Miller DH, Newton MR, van der Poel JC, et al. Magnetic resonance imaging of the optic nerve in optic neuritis. Neurology. Feb 1988;38(2):175-9. [Medline].

  36. Mohamed IG, Roa W, Fulton D, et al. Optic nerve sheath fenestration for a reversible optic neuropathy in radiation oncology. Am J Clin Oncol. Aug 2000;23(4):401-5. [Medline].

  37. Noguera-Pons R, Borrás-Blasco J, Romero-Crespo I, et al. Optic neuritis with concurrent etanercept and isoniazid therapy. Ann Pharmacother. Dec 2005;39(12):2131-5. [Medline].

  38. Noseworthy JH, Lucchinetti C, Rodriguez M, Weinshenker BG. Multiple sclerosis. N Engl J Med. Sep 28 2000;343(13):938-52. [Medline].

  39. Optic Neuritis Study Group. The 5-year risk of MS after optic neuritis. Experience of the optic neuritis treatment trial. Optic Neuritis Study Group. Neurology. Nov 1997;49(5):1404-13. [Medline].

  40. Trip SA, Wheeler-Kingshott C, Jones SJ, et al. Optic nerve diffusion tensor imaging in optic neuritis. Neuroimage. Oct 18 [Epub ahead of print] 2005;[Medline].

  41. Werring DJ, Bullmore ET, Toosy AT, et al. Recovery from optic neuritis is associated with a change in the distribution of cerebral response to visual stimulation: a functional magnetic resonance imaging study. J Neurol Neurosurg Psychiatry. Apr 2000;68(4):441-9. [Medline].

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Keywords

optic neuritis, inflammation of the optic nerve, acute vision loss, multiple sclerosis, human leukocyte antigen Dw2, HLA-Dw2, human leukocyte antigen DR2, HLA-DR2, acute optic neuritis

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Contributor Information and Disclosures

Author

Pil (Peter) S Kang, MD,, Attending Radiologist, Diagnostic Radiology, Department of Diagnostic Radiology, Walter Reed Army Medical Center; Associate Professor, Department of Radiology, Uniformed Services University of Health Sciences
Pil (Peter) S Kang, MD, is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Nothing to disclose.

Coauthor(s)

Fletcher M Munter, MD, Program Director, National Capital Consortium Radiology Residency; Consulting Staff, Department of Radiology, Walter Reed Army Medical Center
Fletcher M Munter, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Neuroradiology, Association of Program Directors in Radiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

Charles Swallow, MD, Department of Radiology, St Marks Hospital
Charles Swallow, MD is a member of the following medical societies: American College of Radiology and American Roentgen Ray Society
Disclosure: Nothing to disclose.

Medical Editor

Barton F Branstetter IV, MD, Associate Professor of Radiology, Otolaryngology, and Biomedical Informatics, University of Pittsburgh; Director of Head and Neck Imaging, Clinical Director of Neuroradiology, Department of Radiology, Division of Neuroradiology, University of Pittsburgh Medical Center
Barton F Branstetter IV, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Roentgen Ray Society, American Society of Neuroradiology, Pennsylvania Medical Society, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

C Douglas Phillips, MD, Director of Head and Neck Imaging, Division of Neuroradiology, Weill Medical College of Cornell University/New York Presbyterian Hospital
C Douglas Phillips, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Society of Head and Neck Radiology, American Society of Neuroradiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Resolution Imaging Medical Corporation
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

James G Smirniotopoulos, MD, Professor of Radiology, Neurology, and Biomedical Informatics, Chairman, Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences
James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

 
 
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