scholarly journals Recurrent Bilateral Optic Neuritis Associated with Myelin Oligodendrocyte Glycoprotein Antibody: A Case Report from Nepal

2021 ◽  
Vol 2021 ◽  
pp. 1-3
Author(s):  
Sangam Shah ◽  
Rajeev Ojha ◽  
Sanjeeta Sitaula ◽  
Dosti Regmi ◽  
Ragesh Karn ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Case Report ◽  
Cell Surface ◽  
Optic Neuritis ◽  
Myelin Sheath ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Inflammatory Condition ◽  
Immune Mediated ◽  
Aquaporin 4 Antibody

Neuromyelitis optica spectrum disorder (NMOSD) is an immune-mediated inflammatory condition involving spinal cord and optic nerves. Diagnosis of NMOSD is done by aquaporin-4 antibody (AQP4) in patients with optic neuritis. Myelin oligodendrocyte glycoprotein (MOG) expressed on the oligodendrocyte cell surface and on the outermost cell surface of the myelin sheath may also be present in patients with NMOSD bilateral optic neuritis. Here, we describe a case of a thirty-nine-year-old-female with recurrent bilateral optic neuritis with positive anti-MOG antibody, and anti-MOG syndrome has not previously been reported from Nepal.

Cortical oscillopsia without nystagmus, an isolated symptom of neuromyelitis optica spectrum disorder with anti-aquaporin 4 antibody

2011 ◽  
Vol 18 (2) ◽  
pp. 244-247 ◽  
Author(s):  
Sung-Min Kim ◽  
Ji-Soo Kim ◽  
Young Eun Heo ◽  
Hye-Ran Yang ◽  
Kyung Seok Park
Keyword(s):  
Spinal Cord ◽  
Neuromyelitis Optica ◽  
Spectrum Disorder ◽  
Aquaporin 4 ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Ocular Manifestation ◽  
Initial Manifestation ◽  
Ocular Symptoms ◽  
Head Tremor ◽  
Aquaporin 4 Antibody

Neuromyelitis optica (NMO), mainly affecting optic nerve and spinal cord, can also manifest diverse ocular symptoms due to brain abnormalities. We present a cortical oscillopsia without nystagmus or head tremor in a patient with neuromyelitis optica spectrum disorder (NMOSD) with anti-aquaporin 4 antibody. This rare ocular manifestation, which is easily underestimated owing to absence of the typical nystagmus, can be an initial manifestation of NMOSD.

scholarly journals CSF levels of glutamine synthetase and GFAP to explore astrocytic damage in seronegative NMOSD

2020 ◽  
Vol 91 (6) ◽  
pp. 605-611
Author(s):  
Iris Kleerekooper ◽  
Megan K Herbert ◽  
H Bea Kuiperij ◽  
Douglas Kazutoshi Sato ◽  
Kazuo Fujihara ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cerebrospinal Fluid ◽  
Glutamine Synthetase ◽  
Glial Fibrillary Acidic Protein ◽  
Optic Neuritis ◽  
Disease Activity ◽  
Similar Pattern ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Csf Levels

ObjectiveTo explore levels of astrocytopathy in neuromyelitis optica spectrum disorder (NMOSD) by measuring levels of the astrocytic enzyme glutamine synthetase (GS) and glial fibrillary acidic protein (GFAP), an established astrocytic biomarker known to be associated with disease activity in multiple sclerosis.MethodsCerebrospinal fluid concentrations of GS and GFAP were measured by ELISA in patients with NMOSD (n=39, 28 aquaporin-4 (AQP4)-Ab-seropositive, 3 double-Ab-seronegative, 4 myelin oligodendrocyte glycoprotein (MOG)-Ab-seropositive and 4 AQP4-Ab-seronegative with unknown MOG-Ab-serostatus), multiple sclerosis (MS) (n=69), optic neuritis (n=5) and non-neurological controls (n=37).ResultsGFAP and GS concentrations differed significantly across groups (both p<0.001), showing a similar pattern of elevation in patients with AQP4-Ab-seropositive NMOSD. GS and GFAP were significantly correlated, particularly in patients with AQP4-Ab-seropositive NMOSD (rs=0.70, p<0.001). Interestingly, GFAP levels in some patients with double-Ab-seronegative NMOSD were markedly increased.ConclusionsOur data indicate astrocytic injury occurs in some patients with double-Ab-seronegative NMOSD, which hints at the possible existence of yet undiscovered astrocytic autoimmune targets. We hypothesise that elevated GS and GFAP levels could identify those double-Ab-seronegative patients suitable to undergo in-depth autoimmune screening for astrocytic antibodies.

Myelin oligodendrocyte glycoprotein antibody-associated optic neuritis mimicking pseudotumor cerebri: A case report

2020 ◽  
Vol 176 (7-8) ◽  
pp. 626-627
Author(s):  
M. Cescutti ◽  
C. Davenas ◽  
C. Tilikete ◽  
F. Durand-Dubief ◽  
R. Marignier ◽  
...  
Keyword(s):  
Case Report ◽  
Optic Neuritis ◽  
Pseudotumor Cerebri ◽  
Myelin Oligodendrocyte Glycoprotein

scholarly journals Neuromyelitis Optica Spectrum Disorder and Anti-MOG Syndromes

Biomedicines ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 42 ◽  
Author(s):  
Marco A. Lana-Peixoto ◽  
Natália Talim
Keyword(s):  
Optic Neuritis ◽  
Neuromyelitis Optica ◽  
Area Postrema ◽  
Water Channel ◽  
Clinical Manifestations ◽  
Transverse Myelitis ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Immunosuppressive Drugs ◽  
Spectrum Disorder ◽  
Neuromyelitis Optica Spectrum Disorder

Neuromyelitis optica spectrum disorder (NMOSD) and anti-myelin oligodendrocyte glycoprotein (anti-MOG) syndromes are immune-mediated inflammatory conditions of the central nervous system that frequently involve the optic nerves and the spinal cord. Because of their similar clinical manifestations and habitual relapsing course they are frequently confounded with multiple sclerosis (MS). Early and accurate diagnosis of these distinct conditions is relevant as they have different treatments. Some agents used for MS treatment may be deleterious to NMOSD. NMOSD is frequently associated with antibodies which target aquaporin-4 (AQP4), the most abundant water channel in the CNS, located in the astrocytic processes at the blood-brain barrier (BBB). On the other hand, anti-MOG syndromes result from damage to myelin oligodendrocyte glycoprotein (MOG), expressed on surfaces of oligodendrocytes and myelin sheaths. Acute transverse myelitis with longitudinally extensive lesion on spinal MRI is the most frequent inaugural manifestation of NMOSD, usually followed by optic neuritis. Other core clinical characteristics include area postrema syndrome, brainstem, diencephalic and cerebral symptoms that may be associated with typical MRI abnormalities. Acute disseminated encephalomyelitis and bilateral or recurrent optic neuritis are the most frequent anti-MOG syndromes in children and adults, respectively. Attacks are usually treated with steroids, and relapses prevention with immunosuppressive drugs. Promising emerging therapies for NMOSD include monoclonal antibodies and tolerization.

scholarly journals Successful treatment of steroid-resistant anti-aquaporin 4 antibody-positive optic neuritis with double-filtration plasmapheresis: a case report

2018 ◽  
Vol 51 (6) ◽  
pp. 379-385
Author(s):  
Kei Fukuda-Hihara ◽  
Masayuki Iyoda ◽  
Tomohiro Saito ◽  
Noriko Arai-Nunota ◽  
Yukihiro Wada ◽  
...  
Keyword(s):  
Case Report ◽  
Optic Neuritis ◽  
Successful Treatment ◽  
Aquaporin 4 ◽  
Steroid Resistant ◽  
Double Filtration Plasmapheresis ◽  
Double Filtration ◽  
Aquaporin 4 Antibody

scholarly journals Mimics of Optic Neuritis in Neuromyelitis Optica Spectrum Disorder: A Case Report

2020 ◽  
pp. 1-5
Author(s):  
Nandita Prabhat ◽  
Karthik Vinay Mahesh ◽  
Aastha Takkar ◽  
Manjul Tripathi ◽  
Chirag Ahuja ◽  
...  
Keyword(s):  
Case Report ◽  
Optic Neuritis ◽  
Neuromyelitis Optica ◽  
Spectrum Disorder ◽  
Neuromyelitis Optica Spectrum Disorder

A Case of Multifocal Neurological Symptoms

2018 ◽  
pp. 9-14
Author(s):  
Aaron E. Miller ◽  
Tracy M. DeAngelis ◽  
Michelle Fabian ◽  
Ilana Katz Sand
Keyword(s):  
Acute Disseminated Encephalomyelitis ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
High Dose ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Good Recovery ◽  
Related Disease ◽  
Demyelinating Disorder ◽  
Immune Mediated ◽  
Initial Onset ◽  
Adolescents And Adults

Acute disseminated encephalomyelitis (ADEM) is an immune-mediated demyelinating disorder characterized by multifocal involvement of the CNS and encephalopathy. Diagnostic criteria also require MRI lesions characteristic for demyelination and that new symptoms/findings not occur more than three months after initial onset. ADEM preferentially affects young children but also occurs in adolescents and adults. An antecedent infection or vaccine may be reported, but a clear causal relationship has not been established, and more often no clear provoking factor is identified. In addition to encephalopathy, patients present with symptoms reflecting multifocal CNS involvement such as optic neuritis, ataxia, hemiparesis, spinal cord syndrome, and seizures. Respiratory failure may occur. ADEM is typically treated with high-dose corticosteroids. Plasma exchange or intravenous immunoglobulin may also be used. The course is most often monophasic with good recovery. However, a subset of patients will go on to have recurrent disease, reflecting a diagnosis of multiple sclerosis, neuromyelitis optica spectrum disorder, or myelin oligodendrocyte glycoprotein related disease.

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