![]() Accordingly, many patients with MOG-EM were falsely classified as having MS in the past. Importantly, however, MOG-EM and MS show a relevant phenotypic, i.e., clinical as well as radiological, overlap : like MS, MOG-EM follows a relapsing course in most cases, at least in adults, and 33 and 15% of adult patients with MOG-EM meet McDonald’s and Barkhof’s criteria for MS, respectively, at least once over the course of disease. ![]() īased on evidence from (a) immunological studies suggesting a direct pathogenic impact of MOG-IgG, (b) neuropathological studies demonstrating discrete histopathological features, (c) serological studies reporting a lack of aquaporin-4 (AQP4)-IgG in almost all MOG-IgG-positive patients, and (d) cohort studies suggesting differences in clinical and paraclinical presentation, treatment response and prognosis, MOG-IgG is now considered to denote a disease entity in its own right, distinct from classic MS and from AQP4-IgG-positive neuromyelitis optica spectrum disorders (NMOSD), which is now often referred to as MOG-IgG-associated encephalomyelitis (MOG-EM). While antibodies to MOG were originally thought to be involved in multiple sclerosis (MS), based on results from enzyme-linked immunosorbent assays employing linearized or denatured MOG peptides as antigen, more recent studies using new-generation cell-based assays have demonstrated a robust association of antibodies to full-length, conformationally intact human MOG protein with (mostly recurrent) optic neuritis (ON), myelitis and brainstem encephalitis, as well as with acute disseminated encephalomyelitis (ADEM)-like presentations, rather than with classic MS. Over the past few years, the role of immunoglobulin G serum antibodies to myelin oligodendrocyte glycoprotein (MOG-IgG) in patients with inflammatory CNS demyelination has been revisited. Finally, we provide recommendations regarding assay methodology, specimen sampling and data interpretation. In addition, we give a list of conditions atypical for MOG-EM (“red flags”) that should prompt physicians to challenge a positive MOG-IgG test result. In this paper, we propose indications for MOG-IgG testing based on expert consensus. To lessen the hazard of overdiagnosing MOG-EM, which may lead to inappropriate treatment, more selective criteria for MOG-IgG testing are urgently needed. However, screening of large unselected cohorts for rare biomarkers can significantly reduce the positive predictive value of a test. Accordingly, increasing numbers of patients with suspected or established MS are currently being tested for MOG-IgG. Owing to a substantial overlap in clinicoradiological presentation, MOG-EM was often unwittingly misdiagnosed as MS in the past. Most experts now consider MOG-IgG-associated encephalomyelitis (MOG-EM) a disease entity in its own right, immunopathogenetically distinct from both classic multiple sclerosis (MS) and aquaporin-4 (AQP4)-IgG-positive neuromyelitis optica spectrum disorders (NMOSD). Over the past few years, new-generation cell-based assays have demonstrated a robust association of autoantibodies to full-length human myelin oligodendrocyte glycoprotein (MOG-IgG) with (mostly recurrent) optic neuritis, myelitis and brainstem encephalitis, as well as with acute disseminated encephalomyelitis (ADEM)-like presentations.
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