Adult Optic Neuritis

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Practice Essentials

Optic neuritis (ON; see the image below) is a demyelinating inflammation of the optic nerve that often occurs in association with multiple sclerosis (MS) and neuromyelitis optica (NMO). A gradual recovery of visual acuity with time is characteristic of optic neuritis,[1] although permanent residual deficits in color vision and contrast and brightness sensitivity are common.[2]



View Image

A case of acute optic neuritis. A. 1.5 Tesla, contrast-enhanced spin echo T1-weighted, fat-suppressed coronal MRI through the orbits shows enlargement....

Signs and symptoms

History

Classically, patients with optic neuritis are young, are often female, and have subacute vision loss associated with pain on eye movement.

The patient’s history may reveal the following signs and symptoms of optic neuritis:

Patients with MS may have recurrent attacks of optic neuritis,[5] which means that a history of previous episodes of decreased vision in the same or fellow eye may be elicited.

NMO is characterized by often severe, bilateral optic neuritis and myelitis in a close temporal relationship.[6, 7, 8, 9] However, optic neuritis can occasionally precede the myelopathy.

Physical examination

Signs of optic neuritis may include the following:

See Clinical Presentation for more detail.

Diagnosis

The following blood tests can be performed when optic neuropathies other than optic neuritis are suspected:

Magnetic resonance imaging (MRI) is highly sensitive for and specific in the assessment of inflammatory changes in the optic nerves, and for central nervous system white matter lesions. MRI also helps to rule out structural lesions.[10, 11]

Visual evoked potentials (VEPs) can be considered in patients with suspected optic neuritis. They may be abnormal even when MRI of the optic nerve is normal. VEPs often show a loss of P100 response in the acute phase. P100 recovers with time, but it usually shows a markedly prolonged latency that persists indefinitely, even after clinical recovery.

See Workup for more detail.

Management

For most patients with optic neuritis, treatment and recovery proceed as follows:

Eculizumab, a monoclonal antibody that targets C5, is the first drug specifically approved by the FDA for adults with neuromyelitis optica spectrum disorder (NMOSD) who are anti-aquaporin-4 (AQP4) antibody–positive.[15]

For patients with optic neuritis whose brain lesions on MRI indicate a high risk of developing clinically definite MS, treatment with immunomodulators (eg, interferon [INF] beta-1a, INF beta-1b, glatiramer acetate) may be considered.[16]

See Treatment and Medication for more detail.

Background

Optic neuritis (ON) is a demyelinating inflammation of the optic nerve that typically first occurs in young adulthood (see the image below). Many cases of optic neuritis are associated with multiple sclerosis (MS) or neuromyelitis optica (NMO), but optic neuritis can occur in isolation.[17] In cases associated with MS, optic neuritis is commonly the first manifestation of the chronic demyelinating process.[18] Long-term follow-up studies have indicated that up to 75% of female patients initially presenting with optic neuritis ultimately develop MS. (See Presentation and Prognosis.)

Occasionally, optic neuritis can result from an infectious process involving the orbits or paranasal sinuses or occur in the course of a systemic viral infection.[19, 20, 21, 22, 23, 24, 25, 26, 27] Certain optic neuropathies, such as anterior ischemic optic neuropathy (AION) and compressive and hereditary optic neuropathies, can resemble optic neuritis.[28]

This article reviews optic neuritis as a primary demyelinating inflammation of the nerve occurring either in isolation or in association with MS or NMO. (NMO is a severe form of a demyelinating disease; it affects the optic nerves and the spinal cord, causing recurrent attacks of blindness and paralysis.[29, 30] ) Much information has been gleaned from the Optic Neuritis Treatment Trial (ONTT), and the reader is encouraged to review the follow-up data from this study. (See Etiology, Treatment, and Medication.)[31, 12, 32, 2]

Patient education

For patient education information, see Multiple Sclerosis.

Etiology

Most cases of optic neuritis are associated with MS, even though optic neuritis can occur in isolation. In MS-associated and isolated, monosymptomatic optic neuritis, the cause is presumed to be an autoimmune reaction that results in a demyelinating inflammation of the nerve. Pathologic studies in patients with optic neuritis associated with MS have shown that the demyelinative lesions in the optic nerve are similar to the MS plaques seen in the brain, with an inflammatory response marked by perivascular cuffing, T cells, and plasma cells. However, little is known about the pathology of isolated optic neuritis.

In a single case of chronic, isolated optic neuritis, a biopsy specimen showed the presence of perivascular lymphocytic infiltration, multifocal demyelination, and reactive astrocytosis in the retrobulbar portion of the optic nerve. Abnormal intrathecal immunoglobulin G (IgG) synthesis, reflected as the presence of oligoclonal bands in the cerebrospinal fluid (CSF), is found in 60-70% of patients with isolated optic neuritis, suggesting an immunologic etiology similar to MS.

NMO has been recognized as a distinct inflammatory demyelinating disease consisting of optic neuritis in combination with longitudinally extensive transverse myelitis. NMO is associated with the presence of a specific serum, NMO IgG autoantibody, which targets the water channel aquaporin-4.[33, 34, 35]

As previously stated, optic neuritis can occasionally result from an infectious process involving the orbits or paranasal sinuses or occur in the course of a systemic viral infection.[19, 20, 21, 22, 23, 24, 25, 26, 27]

Epidemiology

Studies from Sweden and Denmark have reported an annual incidence of 4-5 cases of new-onset optic neuritis per 100,000 persons.[36] Patients living in temperate climates seem to be predisposed to optic neuritis.

Race-, sex-, and age-related demographics

Optic neuritis appears to affect Caucasians more commonly than it does other races. Women are affected twice as often as men.[31]

Typically, patients with first-time, acute optic neuritis are young adults aged 20-45 years. Atypical cases of optic neuritis may be seen in elderly patients. Bilateral optic neuritis in childhood is not uncommon, and it is believed there is less risk of progression to MS.

Prognosis

In contrast to ischemic optic neuropathies and compressive optic neuropathies, a gradual recovery of visual acuity with time is characteristic of optic neuritis.[1] For most patients with optic neuritis, visual function begins to improve 1 week to several weeks after onset, even without any treatment. However, permanent residual deficits in color vision and contrast and brightness sensitivity are common.[2]

Decreased visual acuity secondary to optic neuritis may be permanent. Final visual outcome may be better in patients with an isolated episode of optic neuritis, compared with patients who eventually develop MS. Up to 75% of female patients and 35% of male patients initially presenting with optic neuritis ultimately develop MS.[37, 38, 39]

Patients with silent demyelinative lesions elsewhere in the brain, observed on magnetic resonance imaging (MRI) performed at the initial presentation, are more likely to develop definite MS in the long term than are patients with isolated optic neuritis. In addition, patients who have recurrent episodes of optic neuritis may be more likely to develop MS.

The ten-year risk of developing clinically definite MS following a single episode of optic neuritis was 38% in the entire ONTT study group; the twelve-year risk was 40%. Most of those who developed MS did so within the first five years after the initial episode of optic neuritis.

The strongest predictor of MS in the study group was the presence of brain lesions on MRI at the time of the optic neuritis episode. Within the study group, patients with at least one brain lesion on MRI at the time of the optic neuritis episode had a 56% risk of developing MS within 10 years. Patients with "normal" MRI findings have a 16% risk of progression to clinically definite MS at five-year follow-up, which increases to a 22% risk of developing MS within ten years.

Most patients with relapsing NMO have an aggressive form of the disease that is associated with frequent and severe exacerbations and poor prognosis.

History

A history of preceding viral illness and pain upon eye movement may be present. Typically, patients with first time acute optic neuritis (ON) are otherwise healthy young adults. Patients with optic neuritis experience rapidly developing impairment of vision in 1 eye or, less commonly, both eyes during an acute attack.[3]

Dyschromatopsia (change in color perception) in the affected eye occasionally may be more prominent than the decreased vision.[4] In nearly all cases, the visual changes are associated with a retro-orbital or ocular pain, usually exacerbated by eye movement. The pain may precede the visual loss.

Patients may complain of vision loss exacerbated by heat or exercise (Uhthoff phenomenon). Objects moving in a straight line may appear to have a curved trajectory (Pulfrich phenomenon), presumably due to asymmetrical conduction between the optic nerves.

Patients with MS may have recurrent attacks of optic neuritis.[5] Therefore, a history of previous episodes of decreased vision in the same or the fellow eye may be elicited. A previous history of neurologic problems, such as transient episodes of extremity/facial numbness or weakness, suggests a diagnosis of MS. A family history of MS may exist.

NMO is characterized by optic neuritis and myelitis in a close temporal relationship.[6, 7, 8, 9] However, optic neuritis can occasionally precede the myelopathy. Some patients with NMO develop relapses limited to the optic nerves and spinal cord.

In patients, especially males with bilateral, sequential optic neuropathy with little recovery of vision, exclude Leber hereditary optic neuropathy (LHON). Patients with LHON may have a history of vision loss in maternal uncles.

Chronic relapsing inflammatory optic neuropathy (CRION) is a form of inflammatory optic neuropathy that is frequently bilateral and often painful. It is characterized by relapses and remissions. Brain MRI findings in patients with CRION are normal, and MRI of the optic nerves often, but not always, shows high-signal abnormalities that enhance. The symptoms and signs respond well to corticosteroid treatment, although long‐term immunosuppression is often necessary. The syndrome behaves in a way that is typical of granulomatous optic neuropathy, but, during long-term follow-up, no systemic sarcoidosis is identified.[40]

Physical Examination

In a typical first-time, acute case of optic neuritis, the general physical examination is normal. Pupillary light reaction is decreased in the affected eye and a relative afferent pupillary defect (RAPD) or Marcus Gunn pupil commonly is found. In bilateral cases, the RAPD may not be apparent.

Measurement of visual acuity reveals varying degrees of reduction in vision, from a mildly decreased visual acuity to complete visual loss. However, visual acuity may be normal, with only a limited, mild visual-field defect. Almost all patients with decreased visual acuity also have abnormal contrast sensitivity and color vision, as revealed by examination using a Pelli-Robson chart and Ishihara color plates, respectively.

Classic dictum states that a central scotoma most commonly is seen in optic neuritis. However, the Optic Neuritis Treatment Trial (ONTT) suggested that altitudinal field defects, arcuate defects, and nasal steps were more common than central scotomas and cecocentral scotomas. Visual field examination typically shows a central scotoma. Peripheral extension of the scotoma in any direction, and even a generalized depression of the entire visual field, may be encountered.

In acute optic neuritis, the fundus appears normal because two thirds of cases of optic neuritis are retrobulbar. With time, the optic nerve may become pale.

One third of patients with optic neuritis have a swollen disc (papillitis). The disc edema of optic neuritis often is diffuse. The presence of segmental changes, altitudinal swelling, pallor, arterial attenuation, and splinter hemorrhages suggest other diagnoses (eg, AION).[41]

If a dilated fundus examination is not performed, retinal problems, such as central serous retinopathy and retinal detachment, may be mistaken for optic neuritis.[42]

Patients with NMO often develop a severe, bilateral form of optic neuritis and myelitis. Bitemporal or junctional visual-field defects, indicating chiasm involvement, may be present. Myelitis may be associated with localized back or radicular pain and Lhermitte's sign (spine or limbs paresthesias elicited by neck flexion) early in the course of the disease. Severe degrees of neurologic deficits, including paraplegia, are usual. Symptoms such as respiratory failure or hiccups may occur when the cervical spinal cord lesions extend into the medulla.

Approach Considerations

Blood tests that can be considered to exclude causes of optic neuropathy other than demyelinating optic neuritis (ON) include the following:

However, in a typical case of optic neuritis without any clinical signs or symptoms of a systemic disease, the yield from these tests is extremely low.

CSF analysis often is noncontributory to diagnosis. However, the presence of myelin basic protein, oligoclonal bands, and an elevated IgG index and synthesis rate in the CSF supports the diagnosis of MS. Even in the absence of other signs of MS during the initial presentation, patients with positive findings of demyelination in the CSF are more likely to develop MS in the long term.[43] Neuromyelitis optica (NMO)-IgG is a specific autoantibody marker for NMO.[29, 30]

Formal perimetry should be obtained. Optical coherence tomography can be used to document neuroaxonal loss.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) is highly sensitive and specific in assessing inflammatory changes in the optic nerves (see the image below) and helps to rule out structural lesions. In addition, MRI may have a value in predicting future development of MS in patients presenting with first-time, acute optic neuritis.[44, 10, 45, 46, 11, 47, 48]



View Image

A case of acute optic neuritis. A. 1.5 Tesla, contrast-enhanced spin echo T1-weighted, fat-suppressed coronal MRI through the orbits shows enlargement....

MRI performed at the initial presentation reveals that 10-20% of these patients may have clinically silent demyelinative lesions elsewhere in the brain. MRI at 3.0T is more sensitive to hyperintense lesions than is MRI at 1.5T.[49] These patients are more likely to develop definite MS in the long term than are patients with isolated optic neuritis. The Optic Neuritis Treatment Trial (ONTT) reported the 10-year risk of MS to be 56% with at least 1 MR T2 lesion.[31]

Utilization of fat saturation techniques helps to visualize gadolinium enhancement of the optic nerve and is the best imaging technique to visualize inflammation of the optic nerve.

In addition to MRI of the optic nerves and brain/brainstem, MRI of the spinal cord is indicated in patients with suspected NMO. An MRI of the spinal cord characteristically shows cord swelling, signal changes, and enhancement extending over several levels consistent with longitudinally extensive myelitis.[50]

Visual Evoked Potentials

Visual evoked potentials (VEPs) are an important means of evaluating patients with suspected optic neuritis. They may be abnormal even when MRI of the optic nerve is normal.

VEP often shows a loss of P100 response in the acute phase. P100 recovers with time, but it usually shows a markedly prolonged latency that persists indefinitely even after clinical recovery.

VEP may be abnormal in patients without a past history of optic neuritis, thereby providing evidence of subclinical involvement of the optic nerve. For this reason, VEP often is performed in patients with a suspected diagnosis of MS.

Approach Considerations

Finding professional help early in the course of optic neuritis (ON) is important. The Optic Neuritis Treatment Trial (ONTT) was a carefully performed, randomized, clinical trial that yielded useful information. Despite the ONTT, the treatment of optic neuritis remains somewhat controversial.[13, 12] From a vision standpoint, observation without steroid treatment versus intravenous (IV) steroid treatment showed no difference in ultimate visual outcome at the 5-year mark.[14]

Eculizumab, a monoclonal antibody that targets C5, is the first drug approved by the FDA for adults with neuromyelitis optica spectrum disorder (NMOSD) who are anti-aquaporin-4 (AQP4) antibody–positive. Approval was based on the PREVENT clinical trial. Results showed eculizumab reduced the risk of NMOSD relapse by 94.2% compared with placebo (P< 0.0001). Nearly 98% of eculizumab-treated patients were relapse-free at 48 weeks compared with 63.2% of patients in the placebo arm. Additionally, compared with placebo, eculizumab reduced the adjudicated on-trial annualized relapse rate by 95.5% (P< 0.0001).[15]

Early reports with a small number of patients found some benefit with plasma exchange in acute, severe optic neuritis. Further controlled studies are recommended. In 2016, a randomized controlled trial of erythropoietin in the treatment of optic neuritis was initiated.[51]

Rituximab therapy is considered to be among the most efficient treatments of neuromyelitis optica spectrum disorders (NMOSDs), "even in the absence of class I studies."[52] In a case series of 20 patients with highly relapsing NMO, Kim et al reported significantly reduced relapse rates and clinical stabilization or improvement with mitoxantrone treatment.[53] Further studies conducted in a prospective and controlled fashion are required to determine whether mitoxantrone is a viable treatment option.

Inpatient care

Patients with NMO often require supportive care, as they are prone to many complications, such as deep venous thrombosis, pulmonary embolism, urinary tract infection, decubiti, and contractures related to the myelopathy. Mechanical ventilation may be needed due to respiratory compromise.

Consultations

Consultations with ophthalmology and neurology are recommended for complete evaluation and treatment of suspected optic neuritis cases.

Steroid Therapy

The ONTT protocol used intravenous steroids (methylprednisolone 250 mg qid for 3 days) with oral steroid taper and showed a decreased the short-term risk of development of MS in patients with central nervous system (CNS) white matter plaques, but they had no long-term protective benefit from MS.

IV steroids do little to affect the ultimate visual acuity in patients with optic neuritis, but they do speed the rate of recovery. Some clinicians advocate IV steroids in patients with severe visual loss or bilateral visual loss.

IV steroids are sometimes administered in an outpatient setting or at home. Admission to the hospital is recommended for the duration of high-dose intravenous steroid treatment because of the potential risk of serious adverse effects from this treatment.

The ONTT showed strong evidence against the use of conventional-dose oral steroid monotherapy in the treatment of optic neuritis, since oral steroids alone increased the rate of optic neuritis recurrence.[54, 55]

Medical Care

In patients at high risk of developing MS, consultation with a neurologist for possible immune prophylaxis with beta-interferon or glatiramer acetate should be considered.

Dress polycarbonate safety glasses are an option in patients whose vision does not completely recover.

Medication Summary

Eculizumab, a monoclonal antibody that targets C5, is the first drug specifically approved by the FDA for adults with neuromyelitis optica spectrum disorder (NMOSD) who are anti-aquaporin-4 (AQP4) antibody–positive.[15]

Other pharmacologic therapy in optic neuritis (ON) is directed at ameliorating the acute symptoms of pain and decreased vision caused by demyelinating inflammation of the nerve. Varying regimens of corticosteroids have been used for this purpose. A 3-day course of high-dose IV methylprednisolone followed by a rapid oral taper of prednisone has been shown to provide a rapid recovery of symptoms in the acute phase. (In addition, this treatment may delay the short-term development of MS after optic neuritis.) However, IV steroids do little to affect the ultimate visual acuity in patients with optic neuritis.

For patients with optic neuritis whose brain lesions on MRI indicate a high risk of developing clinically definite MS, treatment with immunomodulators (eg, interferon beta-1a, interferon beta-1b, glatiramer acetate) may be considered.[16] IV immunoglobulin (IVIG) treatment of acute optic neuritis has been shown to have no beneficial effect.

Eculizumab (Soliris)

Clinical Context:  Monoclonal antibody that specifically binds to the complement protein C5 with high affinity, thereby inhibiting its cleavage to C5a and C5b and preventing the generation of the terminal complement complex C5b-9. The precise mechanism by which eculizumab exerts its therapeutic effect in NMOSD is unknown, but is presumed to involve inhibition of aquaporin-4-antibody–induced terminal complement C5b-9 deposition. It is indicated for adults with neuromyelitis optica spectrum disorder (NMOSD) who are anti-aquaporin-4 (AQP4) antibody–positive.

Class Summary

Eculizumab, a monoclonal antibody that targets C5, is the first drug approved by the FDA for treatment of neuromyelitis optica spectrum disorder (NMOSD).

Methylprednisolone (Solu-Medrol, Depo-Medrol, Medrol)

Clinical Context:  Methylprednisolone is a synthetic corticosteroid used intravenously as an anti-inflammatory and immunosuppressant agent. It has been shown to facilitate the recovery of vision in the acute phase of optic neuritis even though it may not change the long-term visual outcome. In addition, treatment with methylprednisolone may delay the development of MS.

Prednisone

Clinical Context:  Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN) leukocyte activity. It is a commonly used oral agent. Prednisone is used for an oral taper of steroids, which may reduce the emotional effects of steroid withdrawal and the risk of the development of adrenocortical insufficiency. However, these risks are not very high after only 3 days of treatment with high-dose steroids, and most neurologists do not use a prednisone taper.

Prednisolone (Pediapred, Prelone, Orapred)

Clinical Context:  Prednisolone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN) leukocyte activity. It is a commonly used oral agent. Prednisolone is used for an oral taper of steroids, which may reduce the emotional effects of steroid withdrawal and the risk of the development of adrenocortical insufficiency. However, these risks are not very high after only 3 days of treatment with high-dose steroids, and most neurologists do not use a prednisone taper.

Class Summary

These have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

What is optic neuritis (ON)?What are the signs and symptoms of optic neuritis (ON)?How is optic neuritis (ON) characterized?What are the physical signs of optic neuritis (ON)?Which blood tests are indicated when optic neuropathies other than optic neuritis (ON) are suspected?Which imaging studies and procedures are indicated in the workup of optic neuritis (ON)?How is optic neuritis (ON) treated?How is adult optic neuritis (ON) characterized?What educational information is available for adults with optic neuritis (ON) and multiple sclerosis (MS)?What causes optic neuritis (ON)?How common is optic neuritis (ON)?What are the demographics of optic neuritis (ON)?What is the prognosis of optic neuritis (ON)?What is the clinical history of optic neuritis (ON)?What are the physical findings in optic neuritis (ON)?Which conditions should be considered in the diagnosis of optic neuritis (ON)?What are the differential diagnoses for Adult Optic Neuritis?What are the approach considerations in the workup of optic neuritis (ON)?When is MRI indicated in the workup of optic neuritis (ON)?How is the visual evoked potentials (VEPs) test used in the workup of optic neuritis (ON)?What are the approach considerations for the treatment of optic neuritis (ON)?When is inpatient care indicated in the treatment of optic neuritis (ON)?Which specialist consultations are indicated in the treatment of optic neuritis (ON)?What is the role of steroid therapy in the treatment of optic neuritis (ON)?What is the medical care for optic neuritis (ON)?Which medications are used in the treatment of optic neuritis (ON)?Which medications in the drug class Monoclonal Antibodies are used in the treatment of Adult Optic Neuritis?Which medications in the drug class Corticosteroids are used in the treatment of Adult Optic Neuritis?

Author

Erhan Ergene, MD, Clinical Assistant Professor, Department of Neurology, University of Illinois College of Medicine at Peoria; Medical Director, Comprehensive Epilepsy Program and Clinical Neurophysiology, Illinois Neurological Institute at OSF Saint Francis Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Reuben M Valenzuela, MD, Clinical Assistant Professor of Neurology, Section of Neuro-ophthalmology, Section of Multiple Sclerosis, Illinois Neurological Institute, University of Illinois College of Medicine Peoria; Neurophthalmologist, OSF HealthCare Illinois Neurological Institute

Disclosure: Nothing to disclose.

Chief Editor

Edsel Ing, MD, MPH, FRCSC, Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Active Staff, Michael Garron Hospital (Toronto East Health Network); Consulting Staff, Hospital for Sick Children and Sunnybrook Hospital, Canada

Disclosure: Nothing to disclose.

Additional Contributors

Nancy A Machens, APN, CNP, Professor of Nursing, Bradley University; Advanced Practice Nurse, Nurse Practitioner, Department of Neurology, Illinois Neurological Institute at OSF Saint Francis Medical Center

Disclosure: Nothing to disclose.

Acknowledgements

Edsel Ing, MD, FRCSC Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Toronto East General Hospital, Canada

Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Ophthalmological Society, North American Neuro-Ophthalmology Society, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Brian R Younge, MD Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of Medscape Reference gratefully acknowledge the assistance of Ryan I Huffman, MD, with the literature review and referencing for this article.

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A case of acute optic neuritis. A. 1.5 Tesla, contrast-enhanced spin echo T1-weighted, fat-suppressed coronal MRI through the orbits shows enlargement and contrast enhancement of the left optic nerve in the retrobulbar portion (arrow). B. Coronal spin echo T1-weighted, fat-suppressed MRI of the same patient shows enlargement and contrast enhancement of the nerve in a parasagittal oblique section (arrow).

A case of acute optic neuritis. A. 1.5 Tesla, contrast-enhanced spin echo T1-weighted, fat-suppressed coronal MRI through the orbits shows enlargement and contrast enhancement of the left optic nerve in the retrobulbar portion (arrow). B. Coronal spin echo T1-weighted, fat-suppressed MRI of the same patient shows enlargement and contrast enhancement of the nerve in a parasagittal oblique section (arrow).

A case of acute optic neuritis. A. 1.5 Tesla, contrast-enhanced spin echo T1-weighted, fat-suppressed coronal MRI through the orbits shows enlargement and contrast enhancement of the left optic nerve in the retrobulbar portion (arrow). B. Coronal spin echo T1-weighted, fat-suppressed MRI of the same patient shows enlargement and contrast enhancement of the nerve in a parasagittal oblique section (arrow).