Retrospective study of consecutive patients who underwent brain/orbit MRI with/without contrast at our institution between 07/01/2019-06/30/2022. Patients with ON T2-hyperintensity or atrophy were included. Medical records were reviewed to determine the etiology, if any, of the T2-hyperintensity and/or atrophy. 

491 patients were included (mean age 52±17 years; 57% men).

381/724 ONs had T2-hyperintensity without atrophy; diagnoses: inflammatory (100), compressive (94), glaucoma (19), multifactorial (47), other (69), unspecified (15), normal (37).

219/724 ONs had T2-hyperintensity and atrophy; diagnoses: inflammatory (36), compressive (50), glaucoma (30), multifactorial (39), other (36), unspecified (12), normal (16).

124/724 ONs had atrophy without T2-hyperintensity; diagnoses: inflammatory (13), compressive (12), glaucoma (32), multifactorial (21), other (24), unspecified (7), normal (15).

68/724 eyes with T2-hyperintensity or atrophy had a normal ophthalmologic examination.

ON T2-hyperintensity on MRI is a non-specific finding; it can be seen in various acute and chronic optic neuropathies. ON T2-hyperintensity with ON atrophy without associated CE can occur secondary to chronic optic neuropathies, such as compressive and glaucomatous optic neuropathies, and is not highly associated with inflammatory optic neuropathies. Therefore, these radiological findings should not automatically prompt an urgent neuro-ophthalmology evaluation or further work-up for optic neuritis, such as a lumbar puncture. However, in the absence of a known cause of the optic neuropathy, an optic neuropathy work-up should be performed.