eMedicine Specialties > Ophthalmology > Optic Nerve

Optic Neuritis, Adult

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
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

Updated: Jul 30, 2009

Introduction

Background

Optic neuritis (ON) is a demyelinating inflammation of the optic nerve. Many cases of ON are associated with multiple sclerosis (MS) or neuromyelitis optica (NMO), but ON can occur in isolation.¹ In cases associated with MS, ON is commonly the first manifestation of the chronic demyelinating process.² Long-term follow-up studies have indicated that up to 75% of female patients initially presenting with ON ultimately develop MS.

Occasionally, ON can be due to an infectious process involving the orbits or paranasal sinuses or occur in the course of a systemic viral infection.^{3,4,5,6,7,8,9,10,11} Certain optic neuropathies, such as anterior ischemic optic neuropathy (AION) and compressive and hereditary optic neuropathies, can resemble ON.¹²

This article reviews ON as a primary demyelinating inflammation of the nerve occurring either in isolation or in association with MS or NMO. 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.

Pathophysiology

In both MS-associated and isolated monosymptomatic ON, the cause is presumed to be an autoimmune reaction, resulting in a demyelinating inflammation of the nerve. Pathological studies in patients with ON 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 ON.

In a single case of chronic isolated ON, 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 ON, suggesting an immunologic pathophysiology similar to MS.

NMO has been recognized as a distinct inflammatory demyelinating disease consisting of ON 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.^13,14

Frequency

United States

See International.

International

Studies from Sweden and Denmark have reported an annual incidence of 4-5 per 100,000 for new onset ON cases.¹⁵

Patients living in temperate climates seem to be predisposed to ON.

Mortality/Morbidity

Decreased visual acuity secondary to optic neuritis may be permanent.

Race

ON appears to affect Caucasians more commonly than other races.

Sex

Women are affected twice as often as men.¹⁶

Age

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

Clinical

History

• Patients with ON experience rapidly developing impairment of vision in one eye or less commonly in both eyes during an acute attack.¹⁷
• Dyschromatopsia (change in color perception) in the affected eye occasionally may be more prominent than the decreased vision.¹⁸ In nearly all cases, the visual changes are associated with a retroorbital 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 asymmetric conduction between the optic nerves.
• Typically, patients with first time acute ON are otherwise healthy young adults.
• A history of preceding viral illness may be present.
• Patients with MS may have recurrent attacks of ON.¹⁹ 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 ON and myelitis in a close temporal relationship.^20,21,22,23 However, ON 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 and optic neuropathy, exclude Leber hereditary optic neuropathy (LHON). Patients with LHON may have a history of vision loss in maternal uncles.

Physical

In a typical first time acute ON case, 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 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 ON. However, the 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 ON, the fundus appears normal because two thirds of cases of ON are retrobulbar. With time, the optic nerve may become pale.
• One third of patients with ON have a swollen disc (papillitis). The disc edema of ON often is diffuse. The presence of segmental changes, altitudinal swelling, pallor, arterial attenuation, and splinter hemorrhages suggest other diagnoses (eg, AION).²⁴
• If a dilated fundus examination is not performed, retinal problems, such as central serous retinopathy and retinal detachment, may be mistaken for ON.
• Patients with NMO often develop a severe and bilateral form of ON 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 neurological deficits, including paraplegia, are usual. Symptoms such as respiratory failure or hiccups may occur when the cervical spinal cord lesions extend into the medulla.

Causes

As noted, most cases of ON are associated with MS even though ON can occur in isolation. In both MS-associated and isolated monosymptomatic ON, the cause is presumed to be an autoimmune reaction, resulting in a demyelinating inflammation of the nerve. NMO is associated with the presence of a specific serum, NMO IgG autoantibody.

Differential Diagnoses

Other Problems to Be Considered

Neuromyelitis optica
Hereditary optic neuropathies
Nutritional optic neuropathies
Wegener granulomatosis
Necrotizing herpetic retinopathy in persons who are immunocompromised

Workup

Laboratory Studies

• Blood tests, such as erythrocyte sedimentation rate, thyroid function tests, antinuclear antibodies, angiotensin-converting enzyme, rapid plasma reagin, and mitochondrial DNA mutation studies can be considered to exclude causes of optic neuropathy other than demyelinating optic neuritis (ON). However, in a typical case of ON without any clinical signs and 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 elevated IgG index and synthesis rate in the CSF supports the diagnosis of MS, and, 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.²⁵
• Neuromyelitis optica-IgG is a specific autoantibody marker for neuromyelitis optica, which is a severe form of a demyelinating disease, likely distinct from MS, that affects the optic nerves and the spinal cord, causing recurrent attacks of blindness and paralysis.^26,27

Imaging Studies

• Magnetic resonance imaging (MRI) is a highly sensitive and specific tool in assessing inflammatory changes in the optic nerves (see Media file 1) 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 ON.^{28,29,30,31,32,33,34} 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 3.0 T is more sensitive to hyperintense lesions than MRI at 1.5 T.³⁵ These patients are more likely to develop definite MS in the long term than patients with isolated ON. The Optic Neuritis Treatment Trial (ONTT) reported the 10-year risk of MS to be 56% with at least one MR T2 lesion.¹⁶
• 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 the MRI of the optic nerves and brain/brainstem, an MRI of the spinal cord is indicated in patients with suspected neuromyelitis optica (NMO). An MRI of the spinal cord characteristically shows cord swelling, signal changes, and enhancement extending over several levels consistent with longitudinally extensive myelitis.³⁶

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).

Other Tests

• Visually-evoked potentials (VEPs) are an important means of evaluating patients with suspected ON and 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 ON, 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.

Treatment

Medical Care

The Optic Neuritis Treatment Trial (ONTT) was a carefully performed randomized clinical trial and yielded useful information. Despite the ONTT, the treatment of optic neuritis (ON) remains somewhat controversial.^37,38 From a vision standpoint, observation without steroid treatment versus intravenous steroid treatment showed no difference in ultimate visual outcome at the 5-year mark.³⁹

The ONTT showed strong evidence against the use of oral steroids in isolation in the treatment of ON, because oral steroids alone caused an increased rate of recurrence of ON.⁴⁰ Intravenous steroids (methylprednisolone 250 mg qid for 3 d with oral steroid taper) decreased the short-term risk of development of MS in patients with CNS white matter plaques, but had no long-term protective benefit from MS. Intravenous steroids do little to affect the ultimate visual acuity in patients with ON, but they do speed the rate of recovery. Some clinicians advocate intravenous steroids in patients with severe visual loss or bilateral visual loss.

Patients with neuromyelitis optica (NMO) often respond to intravenous methylprednisolone. Plasma exchange has been used in patients with no significant improvement with steroids.^41,42

Intravenous 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.

Consultations

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

Medication

Pharmacologic therapy in ON is directed at ameliorating the acute symptoms of pain and decreased vision caused by the demyelinating inflammation of the nerve. Varying regimens of corticosteroids have been used for this purpose. A 3-day course of high-dose intravenous 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 ON. Early reports with a small number of patients found some benefit with plasma exchange in acute, severe ON. Further controlled studies are recommended.

For patients with ON 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.⁴³

IV immunoglobulin (IVIG) treatment of acute ON has been shown to have no beneficial effect.

Corticosteroids

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

Methylprednisolone (Solu-Medrol, Depo-Medrol)

A synthetic corticosteroid used intravenously as an anti-inflammatory and immunosuppressant agent. Has been shown to facilitate the recovery of vision in the acute phase of ON even though it may not change the long-term visual outcome. In addition, treatment with methylprednisolone may delay the development of MS.

Dosing

Adult

1,000 mg/d (an alternative dose is 15 mg/kg/d) for 3 d

Pediatric

Not established

Interactions

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Corticosteroids may exacerbate any intercurrent infection (any infection should be treated adequately before starting high-dose steroids); due to risk of exacerbating any peptic ulcer disease, treatment with an H2 blocker (eg, famotidine) should be considered while patients are on steroids; many patients experience mood changes and fluid retention while on high-dose steroid treatment, but these symptoms resolve after course is finished; many neurologists prefer inpatient treatment because of potentially serious adverse effects, including psychosis, anaphylaxis, hypertension, and hyperglycemia

Prednisone (Deltasone)

Used for an oral taper of steroids, which may reduce emotional effects of steroid withdrawal and risk of developing adrenocortical insufficiency. However, these risks are not very high after only 3 d of treatment with high-dose steroids, and most neurologists do not use a prednisone taper.

Dosing

Adult

1-1.5 mg/kg/d; decrease by 20 mg/d q2-3d

Pediatric

Not established

Interactions

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin infections, connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

Follow-up

Further Inpatient Care

• Patients with neuromyelitis optica (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.

Further Outpatient Care

• Patients should receive follow-up care as needed.

Complications

• Loss of vision from optic neuritis may be permanent.
• Patients with NMO may experience loss of vision as well as residual neurological deficits related to myelopathy.

Prognosis

• In contrast to ischemic optic neuropathies and compressive optic neuropathies, a gradual recovery of visual acuity with time is characteristic of ON.⁴⁴ For most patients with ON, 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.⁴⁵
• Final visual outcome may be better in patients with an isolated episode of ON compared to those patients who eventually develop MS.
  • Up to 75% of female patients and 35% of male patients initially presenting with ON ultimately develop MS.^46,47,48
  • Patients with silent demyelinative lesions elsewhere in the brain, observed on MRI performed at the initial presentation, are more likely to develop definite MS in the long term than patients with isolated ON. In addition, patients who have recurrent episodes of ON may be more likely to develop MS.
  • In patients with normal findings on MRI, a 16% risk of progression to clinically definite MS exists at 5-year follow-up.
• Most patients with relapsing NMO have an aggressive form of the disease that is associated with frequent and severe exacerbations and poor prognosis.

Patient Education

• Finding professional help early in the disease is important.
• For excellent patient education resources, visit eMedicine's Muscle Disorders Center. Also, see eMedicine's patient education article Multiple Sclerosis.

Miscellaneous

Medicolegal Pitfalls

• Attempting to diagnose MS following ON is important.

Multimedia

Media file 1: 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).

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Keywords

adult optic neuritis, ON, optic nerve, multiple sclerosis, MS, neuromyelitis optica, NMO

Contributor Information and Disclosures

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
Erhan Ergene, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Coauthor(s)

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.

Medical Editor

Edsel Ing, MD, FRCSC, Assistant Professor, Department of Ophthalmology & Vision Sciences, University of Toronto: Consulting Staff, Toronto East General Hospital
Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American College of Physician Executives, American Society of Contemporary Ophthalmology, Canadian Ophthalmological Society, Contact Lens Association of Ophthalmologists, North American Neuro-Ophthalmology Society, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
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.

Managing Editor

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.

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

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

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