Editing Optic neuritis (section)

=== Atypical Optic Neuritis ===
ON is classified as atypical optic neuritis when the underlying cause is an etiology other than multiple sclerosis or standalone idiopathic disease. Atypical ON is most frequently seen as an early manifestation of [[neuromyelitis optica spectrum disorder]] (NMOSD), formerly known as neuromyelitis optica (NMO).<ref name=":52">{{Cite journal |last1=Sarkar |first1=Prathama |last2=Mehtani |first2=Amit |last3=Gandhi |first3=H. C. |last4=Dubey |first4=Vinita |last5=Tembhurde |first5=Parag Maroti |last6=Gupta |first6=Mohit Kumar |date=January 2021 |title=Atypical optic neuritis: An overview |journal=Indian Journal of Ophthalmology |volume=69 |issue=1 |pages=27–35 |doi=10.4103/ijo.IJO_451_20 |doi-access=free |issn=1998-3689 |pmc=7926095 |pmid=33323567}}</ref> Other causes of atypical ON include myelin oligodendrocyte glycoprotein-antibody-associated disease (MOGAD), other autoimmune disorders (eg, [[Sarcoidosis]], [[Sjögren's disease|Sjogren syndrome]], [[rheumatoid arthritis]], [[Lupus|systemic lupus erythematosus]]), and infections (Bacterial [<nowiki/>[[Tuberculosis]], [[Syphilis|syphillis]], [[meningitis]], [[Lyme disease|Lyme’s disease]], [[Bartonella]]] or Viral [<nowiki/>[[measles]], [[mumps]], [[rubella]], [[Chickenpox|chicken pox]], [[Herpes simplex virus|herpes]]]).<ref name=":52"/>

==== NMOSD (Formerly NMO) ====
Neuromyelitis optica spectrum disorder (NMOSD) is a disorder consisting of six syndromes that cause inflammation and demyelination of the CNS.<ref name=":6">{{Citation |last1=Shumway |first1=Caleb L. |title=Neuromyelitis Optica Spectrum Disorder (NMOSD) |date=2025 |work=StatPearls |url=https://www.ncbi.nlm.nih.gov/books/NBK572108/ |access-date=2025-03-19 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=34283474 |last2=Patel |first2=Bhupendra C. |last3=Tripathy |first3=Koushik |last4=De Jesus |first4=Orlando}}</ref> The hallmark diagnostic criteria of NMOSD is the presence of the aquaporin-4 immunoglobulin G antibodies (AQP4-IgG) found on serology, which is the underlying aberrancy of this autoimmune condition that engenders its distinction from multiple sclerosis.<ref name=":6" /> Clinical manifestations of NMOSD, such as optic neuritis, occur due to antibody-mediated damage against the aquaporin-4 transmembrane water channels which are found in the foot processes of [[astrocyte]]s at high concentrations within the optic nerve, brainstem, and spinal cord.<ref name=":6" />

==== MOGAD ====
Myelin oligodendrocyte glycoprotein-antibody-associated disease (MOGAD) is an autoimmune condition against the myelin oligodendrocyte glycoprotein (MOG) located on both the myelin sheathe and oligodendrocyte cell surfaces of the CNS.<ref name=":7">{{Cite journal |last1=Sechi |first1=Elia |last2=Cacciaguerra |first2=Laura |last3=Chen |first3=John J. |last4=Mariotto |first4=Sara |last5=Fadda |first5=Giulia |last6=Dinoto |first6=Alessandro |last7=Lopez-Chiriboga |first7=A. Sebastian |last8=Pittock |first8=Sean J. |last9=Flanagan |first9=Eoin P. |date=2022 |title=Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management |journal=Frontiers in Neurology |volume=13 |pages=885218 |doi=10.3389/fneur.2022.885218 |doi-access=free |issn=1664-2295 |pmc=9247462 |pmid=35785363}}</ref> Cell-mediated and complement-mediated inflammation results hallmark findings of perivenous and confluent white matter demyelination.<ref name=":7" />

==== Infection ====
A wide range of attributable infectious etiologies have been found to cause optic neuritis and can arise from varying pathophysiologic mechanisms.<ref name=":52"/> The underlying inflammation and demyelination has been shown to manifest as anterior optic neuritis, retrobulbar optic neuritis (normal [[optic disc]]), neuroretinitis (optic disc [[edema]] with the macular star), or anterior optic neuropathy.<ref name=":52" /> It has been proposed that optic nerve involvement secondary to [[Varicella zoster virus|herpes zoster virus]] infection can arise from direct nerve inflammation or an [[Ischemia|ischemic]] mechanism leading to inflammatory [[thrombosis]].<ref name=":52" /> Optic nerve involvement secondary to [[cytomegalovirus]] (CMV) infection has been proposed to involve a similar mechanism in patients with [[Cytomegalovirus retinitis|CMV retinitis]].<ref>{{Cite journal |last=Mansour |first=A. M. |date=June 1997 |title=Cytomegalovirus optic neuritis |url=https://pubmed.ncbi.nlm.nih.gov/10168894 |journal=Current Opinion in Ophthalmology |volume=8 |issue=3 |pages=55–58 |doi=10.1097/00055735-199706000-00010 |issn=1040-8738 |pmid=10168894}}</ref> The pathogenesis of ON secondary to [[HIV]] has been proposed to arise from autoimmune, vascular, and degenerative ischemic pathways.<ref name=":52" />

==== Other Causes ====
Other etiologies associated with optic neuritis include [[congenital anomalies]], [[glaucoma]], elevated [[intracranial pressure]] (i.e. [[papilledema]]), compression, nutritional and toxic optic neuropathy, trauma, inherited optic neuropathy, or infiltration (eg, [[Neoplasm|neoplastic]] or [[granuloma]]tous).<ref>{{Cite journal |last=Riordan-Eva |first=P. |date=November 2004 |title=Clinical assessment of optic nerve disorders |url=https://www.nature.com/articles/6701575 |journal=Eye |volume=18 |issue=11 |pages=1161–1168 |doi=10.1038/sj.eye.6701575 |pmid=15534601 |issn=1476-5454}}</ref>

When an inflammatory recurrent optic neuritis is not demyelinating, it is called [[chronic relapsing inflammatory optic neuropathy]] (CRION).<ref>{{cite journal |vauthors=Kidd D, Burton B, Plant GT, Graham EM |date=February 2003 |title=Chronic relapsing inflammatory optic neuropathy (CRION) |journal=Brain |volume=126 |issue=Pt 2 |pages=276–284 |doi=10.1093/brain/awg045 |pmid=12538397 |doi-access=free}}</ref>