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In most MS-associated optic neuritis, visual function spontaneously improves over 2–3 months, and there is evidence that corticosteroid treatment does not affect the long term outcome. However, for optic neuritis that is not MS-associated (or atypical optic neuritis) the evidence is less clear and therefore the threshold for treatment with ...
Corticosteroid responsive optic neuritis not associated with demyelinating disease should also be ruled out, including sarcoidosis, systemic lupus erythematosus, or other systemic autoimmune disease. [11] Hereditary causes such as Leber's hereditary optic neuropathy are also part of the differential diagnosis. [12]
Optic neuritis is also commonly associated with periocular pain, phosphenes, and other visual disturbances. Treatment of acute optic neuritis involves corticosteroids, plasmapheresis, and IV immunoglobulins in additions to disease modifying immunotherapies to manage the underlying neuropathology associated with the acute inflammatory episode. [26]
Early initiation of treatment with steroids has been shown to improve vision-related outcomes after acute attacks. [1] [59] However, there is no high-level evidence for steroids affecting long-term outcomes; this treatment strategy was borrowed from that for similar diseases (idiopathic optic neuritis and multiple sclerosis). [59] [58]
Optic neuritis, when combined with the presence of multiple demyelinating white matter brain lesions on MRI, is suspicious for multiple sclerosis. Several causes and clinical courses are possible for the optic neuritis. It can be classified in: Single isolated optic neuritis (SION) relapsing isolated optic neuritis (RION)
Autoimmune optic neuropathy (AON), sometimes called autoimmune optic neuritis, may be a forme fruste of systemic lupus erythematosus (SLE) associated optic neuropathy. AON is more than the presence of any optic neuritis in a patient with an autoimmune process, as it describes a relatively specific clinical syndrome.