Adult Optic Neuritis Workup

  • Author: Erhan Ergene, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Feb 17, 2012
 

Approach Considerations

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

  • Erythrocyte sedimentation rate
  • Thyroid function tests
  • Antinuclear antibodies
  • Angiotensin-converting enzyme
  • Rapid plasma reagin
  • Mitochondrial deoxyribonucleic acid (DNA) mutation studies

However, in a typical case of ON 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.[36] Neuromyelitis optica (NMO)-IgG is a specific autoantibody marker for NMO.[13, 14]

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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 ON.[37, 38, 39, 40, 41, 42, 43]

A case of acute optic neuritis. A. 1.5 Tesla, contA 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).

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.[44] These patients are more likely to develop definite MS in the long term than are patients with isolated ON. The Optic Neuritis Treatment Trial (ONTT) reported the 10-year risk of MS to be 56% with at least 1 MR T2 lesion.[15]

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.[45]

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Visual Evoked Potentials

Visual evoked potentials (VEPs) are an important means of evaluating patients with suspected ON. 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 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.

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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.

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.

Additional Contributors

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).
 
 
 
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