An update on optic neuritis.
Chronic relapsing inflammatory optic neuropathy
MOG antibody-associated disease
Multiple sclerosis
Neuro-ophthalmology
Neuromyelitis optica spectrum disorder
Optic neuritis
Journal
Journal of neurology
ISSN: 1432-1459
Titre abrégé: J Neurol
Pays: Germany
ID NLM: 0423161
Informations de publication
Date de publication:
Oct 2023
Oct 2023
Historique:
received:
09
07
2023
accepted:
30
07
2023
revised:
27
07
2023
medline:
21
9
2023
pubmed:
6
8
2023
entrez:
5
8
2023
Statut:
ppublish
Résumé
Optic neuritis (ON) is the most common cause of subacute optic neuropathy in young adults. Although most cases of optic neuritis (ON) are classified as typical, meaning idiopathic or associated with multiple sclerosis, there is a growing understanding of atypical forms of optic neuritis such as antibody mediated aquaporin-4 (AQP4)-IgG neuromyelitis optica spectrum disorder (NMOSD) and the recently described entity, myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD). Differentiating typical ON from atypical ON is important because they have different prognoses and treatments. Findings of atypical ON, including severe vision loss with poor recovery with steroids or steroid dependence, prominent optic disc edema, bilateral vision loss, and childhood or late adult onset, should prompt serologic testing for AQP4-IgG and MOG-IgG. Although the traditional division of typical and atypical ON can be helpful, it should be noted that there can be severe presentations of otherwise typical ON and mild presentations of atypical ON that blur these traditional lines. Rare causes of autoimmune optic neuropathies, such as glial fibrillary acidic protein (GFAP) and collapsin response-mediator protein 5 (CRMP5) autoimmunity also should be considered in patients with bilateral painless optic neuropathy associated with optic disc edema, especially if there are other accompanying suggestive neurologic symptoms/signs. Typical ON usually recovers well without treatment, though recovery may be expedited by steroids. Atypical ON is usually treated with intravenous steroids, and some forms, such as NMOSD, often require plasma exchange for acute attacks and long-term immunosuppressive therapy to prevent relapses. Since treatment is tailored to the cause of the ON, elucidating the etiology of the ON is of the utmost importance.
Identifiants
pubmed: 37542657
doi: 10.1007/s00415-023-11920-x
pii: 10.1007/s00415-023-11920-x
doi:
Substances chimiques
Myelin-Oligodendrocyte Glycoprotein
0
Autoantibodies
0
Aquaporin 4
0
Immunoglobulin G
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
5113-5126Informations de copyright
© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.
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