The two faces of neuromyelitis optica

@article{Weinshenker2014TheTF,
  title={The two faces of neuromyelitis optica},
  author={Brian G. Weinshenker and Dean M. Wingerchuk},
  journal={Neurology},
  year={2014},
  volume={82},
  pages={466 - 467}
}
Over the past 15 years, it had seemed as if neuromyelitis optica (NMO) might be a distinct and homogeneous subtype of CNS demyelinating disease distinguishable from the heterogeneous assortment of patients captured by the umbrella diagnosis of “multiple sclerosis (MS).” NMO had distinctive clinical, radiologic, and pathologic characteristics, and, in most cases, a highly specific biomarker, aquaporin-4 (AQP4) autoantibodies, was detectable.1 However, recent observations might be interpreted as… 
Seronegative Neuromyelitis Optica Spectrum--the challenges on disease definition and pathogenesis.
TLDR
The clinical features, imaging, and laboratory findings that can be helpful on the diagnostic work-up, and the differences between AQP4 antibody positive and negative patients with NMOSD are discussed, including features ofNMOSD with antibodies against myelin oligodendrocyte glycoprotein.
Autoantibody to MOG suggests two distinct clinical subtypes of NMOSD
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The study suggests that antibodies against MOG might be pathogenic in NMOSD patients and that determination of anti-MOG antibodies maybe instructive for management of NMOSd patients.
Aquaporin-4: A novel diagnostic biomarker for seronegative neuromyelitis optica
TLDR
Comparisons of aquaporin-4 (AQP4) concentrations in the serum of NMO/ NMOSD and MS patients, as well as in controls, are compared to establish whether it can be used as diagnostic biomarker for NMO-IgG and MS.
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  • L. Pandit
  • Medicine, Biology
    Annals of Indian Academy of Neurology
  • 2015
TLDR
The clinical manifestations of neuromyelitis optica spectrum of disorders, biomarkers associated with the disease and magnetic resonance imaging characteristics of brain and spinal cord are described.
Treatment of neuromyelitis optica: state-of-the-art and emerging therapies
TLDR
Current NMO treatments include general immunosuppressive agents, B-cell depletion, and plasma exchange, and therapeutic strategies targeting complement proteins, the IL-6 receptor, neutrophils, eosinophils and CD19—all initially developed for other indications—are under clinical evaluation for repurposing for NMO.
Diagnostics of the neuromyelitis optica spectrum disorders (NMOSD)
TLDR
Essential clinical information on neuromyelitis optica spectrum disorders, indications and limits of anti-AQP4 antibody testing, instructions for result interpretation, and an agreed laboratory protocol (Appendix) are reported for the communicative community of neurologists and clinical pathologists.
Distinction between MOG antibody-positive and AQP4 antibody-positive NMO spectrum disorders
TLDR
Patients with NMOSD with MOG antibodies have distinct clinical features, fewer attacks, and better recovery than patients with AQP4 antibodies or patients seronegative for both antibodies.
Clinical Profile of Anti-Myelin Oligodendrocyte Glycoprotein Antibody Seropositive Cases of Optic Neuritis
TLDR
MOG-Abs may contribute to the heterogeneous clinical picture of optic neuritis, and although visual acuity outcome is favourable, there is a tendency of residual visual field deficit and a possibility of repeated relapses.
Distinction between MOG antibody-positive and AQP4 antibody-positive NMO spectrum disorders
TLDR
Commenting on a p value of <0.0000, Lopez Valle and author Gronseth discuss how low a p rate can go and the conflicting data and many challenges associated with this area of study.
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References

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TLDR
Clinical, laboratory, and imaging features generally distinguish neuromyelitis optica from MS, and patients with relapsing optic neuritis and myelitis may have neuromyeliitis opticas rather than MS.
Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: A multicentre study of 175 patients
TLDR
This study provides an overview of the clinical and paraclinical features of NMOSD in Caucasians and demonstrates a number of distinct disease characteristics in seropositive and seronegative patients.
Myelin-oligodendrocyte glycoprotein antibodies in adults with a neuromyelitis optica phenotype
TLDR
4 patients with an NMO/NMOSD phenotype who had antibodies to MOG appear to have more favorable clinical outcomes than those with typical AQP4 antibody–mediated disease, and MOG antibody titers fell in all 4 patients.
Characteristic brain magnetic resonance imaging abnormalities in central nervous system aquaporin-4 autoimmunity
TLDR
In central nervous system AQP4 autoimmunity, brain MRI abnormalities were more common than is generally appreciated and were characterized by their unique localization and configuration.
Distinction between MOG antibody-positive and AQP4 antibody-positive NMO spectrum disorders
TLDR
Patients with NMOSD with MOG antibodies have distinct clinical features, fewer attacks, and better recovery than patients with AQP4 antibodies or patients seronegative for both antibodies.
Relationship Between NMO-Antibody and Anti–MOG Antibody in Optic Neuritis
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TLDR
NMO-Ab and MOG-Ab could be potential biomarkers to determine visual prognosis in patients with ON and potential in Patients with ON for recovery of vision.
Aquaporin 4 expression and tissue susceptibility to neuromyelitis optica.
TLDR
The relatively high levels of expression and of supramolecular aggregation in the optic nerve and spinal cord may contribute to the predilection of these structures to NMO pathologic changes.
Antibodies to MOG are transient in childhood acute disseminated encephalomyelitis
TLDR
The persistence or disappearance of antibodies to MOG may have prognostic relevance for acute childhood demyelination in patients diagnosed with childhood MS.
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