Adult Optic Neuritis Workup

Updated: Jan 22, 2021
  • Author: Andrew A Dahl, MD, FACS; Chief Editor: Edsel B Ing, MD, MPH, FRCSC, PhD, MA  more...
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Approach Considerations

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

  • Erythrocyte sedimentation rate
  • Thyroid function tests
  • Antinuclear antibody test
  • Measurement of angiotensin-converting enzyme level
  • Rapid plasma reagin test
  • Mitochondrial DNA mutation studies

In a typical patient with ON without any clinical signs or symptoms of systemic disease, however, the yield from these tests is extremely low.

Cerebrospinal fluid (CSF) analysis is often noncontributory to diagnosis; however, the presence of myelin basic protein, oligoclonal bands, and an elevated IgG index and synthesis rate in the CSF support the diagnosis of multiple sclerosis (MS). Even in the absence of other signs or symptoms 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. [44]  Neuromyelitis optica (NMO) IgG is a specific autoantibody marker for NMO. [30, 31]

Formal perimetry should be performed. Optical coherence tomography with nerve fiber layer quantification may 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 and helps to rule out structural lesions. In addition, MRI may have a value in predicting future development of multiple sclerosis (MS) in patients presenting with first-time, acute ON. [10, 11, 45, 46, 47, 48, 49]

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

Magnetic resonance imaging performed at the initial presentation reveals that 10-20% of these patients may have clinically silent demyelinated lesions elsewhere in the brain. Magnetic resonance imaging at 3.0T is more sensitive to hyperintense lesions than MRI at 1.5T. [50]  These patients are far more likely to develop definite MS in the long term than are patients with isolated ON. In the Optic Neuritis Treatment Trial (ONTT), researchers reported the 10-year risk for MS to be 56% with at least 1 MR T2 lesion. [32]

Use of fat saturation techniques helps to visualize gadolinium enhancement of the optic nerve and is the best imaging technique with which 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 neuromyelitis optica. An MRI of the spinal cord characteristically shows cord swelling, signal changes, and enhancement extending over several levels, which is consistent with longitudinally extensive myelitis. [51]


Visual Evoked Potentials

Visual evoked potentials (VEPs) are an important means of evaluating patients with suspected optic neuritis (ON). They may be abnormal even when MRI of the optic nerve reveals no abnormalities.

Visual evoked potentials 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.

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