Different etiologies and prognoses of optic neuritis in demyelinating diseases

Akaishi, Tetsuya; Nakashima, Ichiro; Takeshita, Takayuki; Kaneko, Kimihiko; Mugikura, Shunji; Sato, Douglas Kazutoshi; Takahashi, Toshiyuki; Nakazawa, Toru; Akiyama, Masashi; Fujihara, Kazuo

doi:10.1016/j.jneuroim.2016.09.007

Cited by 59 publications

(43 citation statements)

References 14 publications

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“…Optic neuritis is probably the most common clinical phenotype of MOG‐IgG‐associated disease. It can be unilateral or simultaneous bilateral, but in contrast to AQP4‐IgG‐positive optic neuritis, optic chiasmal involvement is rare . In the acute phase, severe visual impairment occurs, but functional recovery is relatively good, and unlike AQP4‐IgG‐positive optic neuritis, blindness is uncommon in MOG‐IgG‐positive optic neuritis.…”

Section: Clinical Phenotypes Of Mog‐igg‐associated Diseasementioning

confidence: 99%

Myelin oligodendrocyte glycoprotein immunoglobulin G‐associated disease: An overview

Fujihara

Sato

Nakashima

et al. 2018

Clinical & Exp Neuroim

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Myelin oligodendrocyte glycoprotein (MOG) is localized at the outermost layer of the myelin sheath and is accessible for autoantibodies. Although experimental autoimmune encephalitis induced with MOG immunization has been studied for 30 years, the results of previous reports on MOG immunoglobulin G (IgG) detection with enzyme-linked immunosorbent assay and Western blot are confusing. However, after the development of human MOG-transfected cell-based assay to detect conformational-sensitive MOG-IgG, unique groups of patients have been found seropositive, and MOG-IgG-associated disease has become a hot topic in clinical neuroimmunology. Currently, the clinical spectrum of MOG-IgG-associated disease includes idiopathic optic neuritis, acute disseminated encephalomyelitis, encephalitides (brainstem and cerebral cortical), idiopathic myelitis, atypical multiple sclerosis, aquaporin-4 IgG-negative neuromyelitis optica spectrum disorders and others. MOG-IgG-associated disease occurs in both children and adults, and the female:male ratio is almost 1:1. Pleocytosis in the cerebrospinal fluids during acute exacerbation is often seen, but oligoclonal IgG bands are usually negative. T helper cell 17, B cells and neutrophil-related cytokines appear to be upregulated intrathecally. The pathology of acute lesions is characterized by active inflammation demyelination with deposition of immunoglobulins and complements. Just like aquaporin 4 IgG-positive neuromyelitis optica spectrum disorders, some disease-modifying drugs for multiple sclerosis seem to be inefficacious in MOG-IgG-associated disease, and chronic immunosuppression is required to prevent relapse, especially in patients persistently positive for MOG-IgG. Our understanding of this newly recognized disease remains insufficient, and the progress of research is much expected.

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Section: Clinical Phenotypes Of Mog‐igg‐associated Diseasementioning

confidence: 99%

Myelin oligodendrocyte glycoprotein immunoglobulin G‐associated disease: An overview

Fujihara

Sato

Nakashima

et al. 2018

Clinical & Exp Neuroim

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“…Seropositivity for MOG autoantibodies, which was determined with a cell‐based assay, is present in patients with several CNS autoimmune disorders, including optic neuritis, acute disseminated encephalomyelitis, multiphasic disseminated encephalitis, NMOSD with AQP4 antibody seronegativity and anti‐NMDA receptor encephalitis . Among these, patients with optic neuritis who are positive for MOG antibodies are characterized by an equal gender ratio, younger onset age, longer lesions with swelling on magnetic resonance imaging and better prognoses of visual function, compared with patients with optic neuritis who are positive for AQP4 autoantibodies . Further studies are required to elucidate the pathogenic roles of MOG autoantibodies in CNS autoimmune disorders.…”

Section: Clinical Features Of Autoimmune Optic Neuritismentioning

confidence: 99%

Clinical characteristics of autoimmune optic neuritis

Kawachi

2017

Clinical & Exp Neuroim

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Autoimmune disorders of the central nervous system often involve autoimmune inflammation of the anterior visual pathways. Autoimmune optic neuritis can be categorized as: (i) isolated optic neuritis; (ii) relapsing isolated optic neuritis: (iii) chronic relapsing inflammatory optic neuropathy; (iv) neuromyelitis optica spectrum disorders-associated optic neuritis; or (v) multiple sclerosis-associated optic neuritis. Studies of serum-specific autoantibodies, such as aquaporin-4 and myelin oligodendrocyte glycoprotein, have revealed some underlying mechanisms of autoimmune optic neuritis. However, the etiology and pathogenesis of most cases of autoimmune optic neuritis remain unclear. The following clinical features of autoimmune optic neuritis are profoundly affected by the unique structure of the human anterior visual pathways: (i) vulnerability to swelling of the intracanalicular optic nerve as a result of the limited space within the bony canal; (ii) inflammatory cell infiltration through the subarachnoid space, pia and pial septa; (iii) compartmentalized dynamics of cerebrospinal fluid as a result of the culde-sac anatomy of the optic nerve; (iv) permeability of the prelaminar optic nerve head as a result of the lack of classical blood-brain barrier characteristics; and (v) retinal abnormalities, which are a diagnostic window of neurodegenerative processes of the optic nerves and/or brain. Future studies are required to configure a systemic nosology for optic neuritis with international consensus, elucidate specific diagnostic biomarkers, carry out clinical trials of the acute and chronic phases of the disease etiologies, and elucidate possible neuroprotective and remyelinating treatments.

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“…However, bilateral, simultaneous and revealing presentations of the disease remain exceptional and unusual [3,4]. We report an observation.…”

Section: Introductionmentioning

confidence: 83%

“…The etiological diagnosis of this optic neuropathy represents a real challenge for the clinician given the multitude of possible causes. Among the demyelinating neuropathies most frequently involved are multiple sclerosis, neuromyelitis optica (previously known as Devic's disease), neuromyelitis optica spectrum disorders (NMOSD, specifically associated with anti-aquaporin-4 antibodies) and anti-myelin oligodendrocyte glycoprotein (MOG) autoantibodies-related demyelinating diseases [1,4]. The so-called "idiopathic" optical neuritis has become increasingly rare since the detection of these specific entities associated with the auto-antibodies mentioned above [4].…”

Section: Introductionmentioning

confidence: 99%

Bilateral and Simultaneous Retrobulbar Optic Neuritis Revealing Multiple Sclerosis

Bouomrani¹,

Belgacem²,

Rekik³

et al. 2017

J Mult Scler

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Optic neuritis is a common manifestation of multiple sclerosis. It occurs in two thirds of patients at some point in the course of this disease and is usually unilateral, acute and often recurrent. However, optic neuritis can be the first manifestation of this demyelinating disease in 15 to 20% of cases.Bilateral, simultaneous and retrobulbar forms of optic neuritis inaugurating multiple sclerosis remain exceptional and unusual. They represent a real diagnostic challenge and require special attention from the clinician Herein we report the case of bilateral simultaneous and isolated retrobulbar optic neuritis inaugurating multiple sclerosis in a 24 year old woman.

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Different etiologies and prognoses of optic neuritis in demyelinating diseases

Cited by 59 publications

References 14 publications

Myelin oligodendrocyte glycoprotein immunoglobulin G‐associated disease: An overview

Myelin oligodendrocyte glycoprotein immunoglobulin G‐associated disease: An overview

Clinical characteristics of autoimmune optic neuritis

Bilateral and Simultaneous Retrobulbar Optic Neuritis Revealing Multiple Sclerosis

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