eMedicine Specialties > Radiology > Head/Neck

Optic Neuritis: Imaging

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

Magnetic Resonance Imaging


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 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 fat-suppressed postgadolinium T1-weighted image through the orbit reveals an intensely enhancing segment of the distal left optic nerve (corresponding to the site of subtle increased signal on the image in Image 1 in Multimedia).

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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 fat-suppressed postgadolinium T1-weighted image through the orbit reveals an intensely enhancing segment of the distal left optic nerve (corresponding to the site of subtle increased signal on the image in Image 1 in Multimedia).



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. Coronal fat-suppressed postgadolinium T1-weighted image demonstrates intense enhancement within the optic nerve (same patient as Images 1-2 in Multimedia). No significant nerve expansion or enhancement of the adjacent tissues is seen. Note the normal right optic nerve for comparison.

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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. Coronal fat-suppressed postgadolinium T1-weighted image demonstrates intense enhancement within the optic nerve (same patient as Images 1-2 in Multimedia). No significant nerve expansion or enhancement of the adjacent tissues is seen. Note the normal right optic nerve for comparison.



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.



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 fluid-attenuation inversion recovery image demonstrates bilateral periventricular white matter lesions. Several additional and similar lesions were seen in other locations (not shown). No history of prior neurologic illness was noted in the patient, but in the setting of acute optic neuritis, the multiple white matter lesions in a number and pattern atypical for patient age were considered supportive of the diagnosis of multiple sclerosis (same patient as Image 4 in Multimedia).

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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 fluid-attenuation inversion recovery image demonstrates bilateral periventricular white matter lesions. Several additional and similar lesions were seen in other locations (not shown). No history of prior neurologic illness was noted in the patient, but in the setting of acute optic neuritis, the multiple white matter lesions in a number and pattern atypical for patient age were considered supportive of the diagnosis of multiple sclerosis (same patient as Image 4 in Multimedia).


Findings

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.5

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.6

Patients in the Optic Neuritis Treatment Trial, who were enrolled between July 1, 1988, and June 30, 1991, 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.41

False Positives/Negatives

Although not specifically relevant to optic neuritis, false-positive results in orbital imaging can result from failure of complete fat saturation related to magnetic susceptibility artifact from dental amalgam and air–soft tissue interfaces, particularly at the inferior margin of the orbit. This is true especially for frequency-selective fat-saturation techniques but less so for inversion recovery sequences.

Fat-saturation failure can mimic orbital edema on multiecho train T2-weighted images or enhancement on fat-suppressed T1-weighted images. Careful evaluation of the tissue surrounding the orbit should reveal the true cause of signal distortion. This artifact should not occur in optic neuritis because the lesion of optic neuritis is confined to the nerve but, potentially, it can mislead the interpreter to conclude that more diffuse orbital inflammation is the cause of vision loss.

Occasionally, the enhancement pattern in optic neuritis may be a peripheral tram-track pattern. Potentially, this can be confused with the enhancement pattern of optic nerve meningioma; however, the optic neuritis pattern should be distinguished from the meningioma pattern by enhancement limited to the nerve, rather than the sheathlike pattern of meningioma, by the absence of significant mass or expansion, and by the clinical features of acute onset vision loss and pain.

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

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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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