Cerebrospinal fluid findings in patients with myelin oligodendrocyte glycoprotein (MOG) antibodies. Part 1: Results from 163 lumbar punctures in 100 adult patients

Medientyp: E-Artikel
Titel: Cerebrospinal fluid findings in patients with myelin oligodendrocyte glycoprotein (MOG) antibodies. Part 1: Results from 163 lumbar punctures in 100 adult patients
Beteiligte: Jarius, Sven; Pellkofer, Hannah; Siebert, Nadja; Korporal-Kuhnke, Mirjam; Hümmert, Martin W.; Ringelstein, Marius; Rommer, Paulus S.; Ayzenberg, Ilya; Ruprecht, Klemens; Klotz, Luisa; Asgari, Nasrin; Zrzavy, Tobias; Höftberger, Romana; Tobia, Rafik; Buttmann, Mathias; Fechner, Kai; Schanda, Kathrin; Weber, Martin; Asseyer, Susanna; Haas, Jürgen; Lechner, Christian; Kleiter, Ingo; Aktas, Orhan; Trebst, Corinna; [...]
Erschienen: Springer Science and Business Media LLC, 2020
Erschienen in: Journal of Neuroinflammation
Sprache: Englisch
DOI: 10.1186/s12974-020-01824-2
ISSN: 1742-2094
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Beschreibung: <jats:title>Abstract</jats:title><jats:sec> <jats:title>Background</jats:title> <jats:p>New-generation cell-based assays have demonstrated a robust association of serum autoantibodies to full-length human myelin oligodendrocyte glycoprotein (MOG-IgG) with (mostly recurrent) optic neuritis, myelitis, and brainstem encephalitis, as well as with neuromyelitis optica (NMO)-like or acute-disseminated encephalomyelitis (ADEM)-like presentations. However, only limited data are yet available on cerebrospinal fluid (CSF) findings in MOG-IgG-associated encephalomyelitis (MOG-EM; also termed MOG antibody-associated disease, MOGAD).</jats:p> </jats:sec><jats:sec> <jats:title>Objective</jats:title> <jats:p>To describe systematically the CSF profile in MOG-EM.</jats:p> </jats:sec><jats:sec> <jats:title>Material and methods</jats:title> <jats:p>Cytological and biochemical findings (including white cell counts and differentiation; frequency and patterns of oligoclonal bands; IgG/IgM/IgA and albumin concentrations and CSF/serum ratios; intrathecal IgG/IgA/IgM fractions; locally produced IgG/IgM/IgA concentrations; immunoglobulin class patterns; IgG/IgA/IgM reibergrams; Link index; measles/rubella/zoster (MRZ) reaction; other anti-viral and anti-bacterial antibody indices; CSF total protein; CSF <jats:sc>l</jats:sc>-lactate) from 163 lumbar punctures in 100 adult patients of mainly Caucasian descent with MOG-EM were analyzed retrospectively.</jats:p> </jats:sec><jats:sec> <jats:title>Results</jats:title> <jats:p>Most strikingly, CSF-restricted oligoclonal IgG bands, a hallmark of multiple sclerosis (MS), were absent in almost 90% of samples (<jats:italic>N</jats:italic> = 151), and the MRZ reaction, the most specific laboratory marker of MS known so far, in 100% (<jats:italic>N</jats:italic> = 62). If present, intrathecal IgG (and, more rarely, IgM) synthesis was low, often transient and mostly restricted to acute attacks. CSF WCC was elevated in > 50% of samples (median 31 cells/μl; mostly lymphocytes and monocytes; > 100/μl in 12%). Neutrophils were present in > 40% of samples; activated lymphocytes were found less frequently and eosinophils and/or plasma cells only very rarely (< 4%). Blood–CSF barrier dysfunction (as indicated by an elevated albumin CSF/serum ratio) was present in 48% of all samples and at least once in 55% of all patients (<jats:italic>N</jats:italic> = 88) tested. The frequency and degree of CSF alterations were significantly higher in patients with acute myelitis than in patients with acute ON and varied strongly depending on attack severity. CSF <jats:sc>l</jats:sc>-lactate levels correlated significantly with the spinal cord lesion load in patients with acute myelitis (<jats:italic>p</jats:italic> < 0.0001). Like pleocytosis, blood–CSF barrier dysfunction was present also during remission in a substantial number of patients.</jats:p> </jats:sec><jats:sec> <jats:title>Conclusion</jats:title> <jats:p>MOG-IgG-positive EM is characterized by CSF features that are distinct from those in MS. Our findings are important for the differential diagnosis of MS and MOG-EM and add to the understanding of the immunopathogenesis of this newly described autoimmune disease.</jats:p> </jats:sec>
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