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Published on: September 4, 2021
Chronic optic neuropathy: correlating MR imaging features and etiology
Steven Cajamarca1, Rohini N Nadgir2, Suyang Li1
1Departments of Radiology and Ophthalmology. Boston Medical Center, Boston University Chobanian & Avedisian School of Medicine, Boston, United States.
Background And Purpose:
Chronic optic neuropathy (CON) represents a final common pathway of sustained optic nerve injury from diverse etiologies, yet characteristic MRI features and their clinical correlations are not well defined. This study evaluated the predominant MR imaging findings of non-compressive CON and correlated these patterns with underlying clinical etiologies.
Materials And Methods:
We retrospectively identified 186 patients with MRI reports referencing chronic optic neuritis or neuropathy from 2009 to 2024. Of these, 162 met inclusion criteria, defined as high-resolution orbital MRI and ophthalmologic confirmation of CON. Three reviewers assessed optic nerve caliber, T2/FLAIR signal abnormality, and post-contrast enhancement. Ophthalmologic records were reviewed to determine clinical laterality and etiology.
Results:
Among 162 patients, 66 (40.7%) demonstrated bilateral and 96 (59.3%) unilateral MRI findings. The predominant imaging pattern across etiologies was optic nerve atrophy (< 3 mm) with increased T2/FLAIR signal, present in 125 patients. Enhancement was rare (n = 7). Laterality mismatches were frequent: 42 patients (25.9%) demonstrated bilateral MRI findings despite unilateral clinical involvement, while 13 (8.0%) had bilateral clinical disease with unilateral imaging abnormalities. The leading etiologies were multiple sclerosis (20.0%), glaucoma (16.7%), unspecified optic neuritis (13.0%), and post-traumatic injury (5.5%). Across all etiologies, chronic changes were characterized by atrophy with or without T2/FLAIR hyperintensity. Enhancement, when present, was associated with recent or subacute demyelination.
Conclusion:
Optic nerve atrophy with increased T2/FLAIR signal and absent enhancement constitutes the dominant MRI pattern of non-compressive CON, most likely reflecting chronic axonal degeneration rather than active inflammation. These findings reliably indicate chronic optic nerve injury but have limited specificity for etiology. Frequent imaging and clinical laterality discrepancies suggest subclinical or asymmetric disease. MRI should therefore be interpreted in conjunction with ophthalmologic evaluation when determining the underlying cause of CON.
