Matiello, M. et al. NMO-IgG predicts the outcome of recurrent optic neuritis. Neurology 70, 2197-2200

Department of Neurology, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905, USA.
Neurology (Impact Factor: 8.29). 07/2008; 70(23):2197-200. DOI: 10.1212/01.wnl.0000303817.82134.da
Source: PubMed


To determine the prognostic value of neuromyelitis optica (NMO)-immunoglobulin G (IgG) in patients with recurrent optic neuritis (ON). The aquaporin-4-specific serum autoantibody, NMO-IgG, is a biomarker for NMO and relapsing transverse myelitis. Recurrent ON may herald multiple sclerosis (MS) or NMO, or it may occur as an isolated syndrome. The prognosis and response to therapy differs in each of these contexts.
We evaluated 34 patients who were tested for NMO-IgG between 2000 and 2007 and who had two or more episodes of ON without satisfying a diagnosis of MS or NMO prior to serologic testing. Clinical data were available for 25 Mayo Clinic patients (5 NMO-IgG positive and 20 NMO-IgG negative) and for an additional 9 seropositive patients whose serum was referred to the Mayo Clinic Neuroimmunology laboratory for testing.
Twenty percent of the patients with recurrent ON seen at Mayo Clinic were seropositive. All NMO-IgG-positive patients (vs 65% NMO-IgG-negative patients) had at least one attack with visual acuity in the affected eye worse than 20/200 (p = 0.05). In seropositive patients for whom long-term follow-up was possible (median 8.9 years after the initial ON), 6 of 12 (50%) experienced an episode of myelitis and fulfilled criteria for NMO. In contrast, 1 of 15 seronegative patients (6.7%) fulfilled McDonald criteria for MS (p = 0.03). Seropositive patients had a final visual score which was worse than that of seronegative patients (p = 0.02).
Neuromyelitis optica (NMO)-immunoglobulin G seropositivity predicts poor visual outcome and development of NMO. Seropositive recurrent optic neuritis is a limited form of NMO.

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Available from: Anu Jacob, Jan 10, 2014
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    • "Inflammatory cells then enter the lesion causing further tissue injury including demyelination and axonal damage. In AQP4-IgG NMO patients, recovery after an attack is usually limited [7-9]. "
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    ABSTRACT: Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG. MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks. These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients.
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    • "For long time, NMO was thought to be a variant of multiple sclerosis (MS), although the prognosis and the response to the therapy was different [1]. The identification of a specific serum autoantibody marker by tissue-based indirect immunofluorescence (IIF), NMO-IgG, that bound to astrocytic membranes and the recognition of the target antigen as the water channel aquaporin-4 (AQP4) [2], led to expand the clinical spectrum of NMO to limited forms of the disease, to define a new set of diagnostic criteria, and to expedite the diagnosis and treatment of the patients [1,3,4,5,6,7,8]. "
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    PLoS ONE 11/2013; 8(11):e79083. DOI:10.1371/journal.pone.0079083 · 3.23 Impact Factor
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    • "The three supportive criteria are contiguous spinal cord MRI lesion extending over ≤3 vertebral segments, brain MRI not meeting the diagnostic criteria for multiple sclerosis (MS), and seropositive NMO-IgG4,11,13,27). The diagnosis and prognosis of NMO are different from MS. Early aggressive treatment of NMO may be more efficient in preventing permanent neurologic deficit than early treatment of MS3,26,28). "
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