Neuropediatrics 2016; 47 - PS01-17
DOI: 10.1055/s-0036-1583609

Role of MOG Antibodies in the Differential Diagnosis of Acquired Demyelinating CNS Syndromes in Children

E. Hennes 1, M. Baumann 2, M. Schimmel 3, M. Karenfort 4, M. Häusler 5, B. Bajer-Kornek 6, A. Blaschek 7, S. Leiz 8, T. Gotwald 9, T. Berger 10, M. Reindl 10 K. Rostasy 11and the BIOMARKER Study Group
  • 1Department of Pediatrics, Olgahospital, Stuttgart/Germany
  • 2Division of Pediatric Neurology, Department of Pediatrics I, Innsbruck Medical University, Innsbruck, Austria
  • 3Children’s Hospital, Städtische Kliniken Augsburg, Augsburg, Germany
  • 4Department of General Pediatrics, Pediatric Neurology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany
  • 5Division of Neuropediatrics and Social Pediatrics, Department of Pediatrics, University Hospital, RWTH Aachen, Germany
  • 6Department of Neurology, Medical University of Vienna, Vienna, Austria
  • 7Department of Pediatric Neurology and Developmental Medicine, Dr. von Hauner’s Children’s Hospital, University of Munich, Munich, Germany
  • 8Division of Pediatric Neurology, Department of Pediatrics, Klinikum Dritter Orden, Munich, Germany
  • 9Radiological Institute, Sanatorium Kettenbrücke, Innsbruck, Austria
  • 10Clinical Dept. of Neurology, Innsbruck Medical University, Innsbruck, Austria
  • 11Department of Pediatric Neurology, Vestische Kinder- und Jugendklinik Datteln, Datteln, Germany

Background: MOG antibodies have been recently reported in recurrent ON, ADEM and AQP4 negative NMO, but less frequently in MS. Objective was to assess the prognostic value of MOG antibodies in the differential diagnosis of first acute inflammatory and demyelinating events alone and in combination with markers (e.g., OCBs, CSF cell count). In this prospective multicenter hospital based study, clinical course, CSF- and MRI studies, outcome, MOG-,AQP4-, and EBV- antibody status of 252 children with a first demyelinating event and a follow up of at least two years were reviewed.

Methods: In our cohort of 252 children 84 had a final diagnosis of MS, CIS (n = 56), ADEM (n = 45), recurrent forms such as ADEMON/MDEM) (n = 10), NMO or limited forms (NMOSD) (n = 20) and recurrent ON (n = 13). 24 children were diagnosed with other neurological diseases. MOG antibodies were predominately found in children with ADEM, NMO, LETM, bilateral ON and children who developed further demyelinating episodes including ADEMON/MDEM. MOG antibodies were not detected in children with CIS with an MRI showing typical MS lesions or in patients subsequently diagnosed with MS. MOG antibodies in CIS/ON were present only in children who had an ADEM-like MRI, affecting the optic nerve or in a subgroup of children who developed further episodes of ON.

Conclusion: The presence of MOG antibodies pleads strongly against diagnosis of MS. Patients with high and persisting antibodies tend to have further demyelinating events (e.g., ON, NMO). A distinct pathogenesis in patients with acute demyelinating syndrome and MOG antibodies can be assumed.