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Clinical and neuroradiological differences of paediatric acute disseminating encephalomyelitis with and without antibodies to the myelin oligodendrocyte glycoprotein.
J Neurol Neurosurg Psychiatry. 2015 Mar; 86(3):265-72.JN

Abstract

BACKGROUND

Myelin oligodendrocyte glycoprotein (MOG) antibodies have been recently described in children with acute disseminating encephalomyelitis (ADEM), but the clinical and neuroradiological characterisation of this subgroup is lacking.

OBJECTIVE

To compare the clinical and neuroradiological features of paediatric ADEM with and without MOG antibodies.

METHODS

Clinical course, cerebrospinal fluid (CSF)-, MRI studies, outcome and MOG status of 33 paediatric ADEM prospectively studied were reviewed.

RESULTS

MOG antibodies (median 1:2560; range 1:160-1:20 480) were detected in 19 children with ADEM. The majority of children showed a decline of serum MOG-IgG titres over time. Children with MOG antibodies did not differ in their age at presentation, sex ratio, the presence of oligoclonal bands, clinical symptoms or initial severity, apart from a higher CSF cell count (p=0.038), compared with children without MOG antibodies. In addition, further relapsing demyelinating episodes associated with MOG antibodies were observed only in children with MOG antibodies. All 19 children with MOG antibodies had a uniform MRI pattern, characterised by large, hazy and bilateral lesions and the absence of atypical MRI features (eg, mainly small lesions, well-defined lesions), which was significantly different compared to that of children without MOG antibodies (p=0.003; and p=0.032, respectively). In addition, children with MOG antibodies had involvement of more anatomical areas (p=0.035) including the myelon characterised by a longitudinally extensive transverse myelitis (p=0.003), more often a complete resolution of lesions (p=0.036) and a better outcome (p=0.038).

CONCLUSIONS

Patients with ADEM with MOG antibodies in our cohort had a uniform MRI characterised by large, bilateral and widespread lesions with an increased frequency of longitudinal extensive transverse myelitis and a favourable clinical outcome in contrast to children lacking MOG antibodies.

Authors+Show Affiliations

Division of Pediatric Neurology, Department of Pediatrics I, Innsbruck Medical University, Innsbruck, Austria.Division of Pediatric Neurology, Department of Pediatrics I, Innsbruck Medical University, Innsbruck, Austria.Division of Pediatric Neurology, Department of Pediatrics I, Innsbruck Medical University, Innsbruck, Austria.Division of Pediatric Neurology, Department of Pediatrics I, Innsbruck Medical University, Innsbruck, Austria Clinical Department of Neurology, Klinikum Bogenhausen, Munich, Germany.Clinical Department of Neurology, Innsbruck Medical University, Innsbruck, Austria.Clinical Department of Neurology, Innsbruck Medical University, Innsbruck, Austria The Feinstein Institute for Medical Research, Center for Autoimmune and Musculoskeletal Diseases, Manhasset, New York, USA.Department of General Pediatrics, Pediatric Neurology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.Behandlungszentrum Vogtareuth, Vogtareuth, Germany.Department of Pediatrics, Division of Neuropediatrics and Social Pediatrics, University Hospital, Aachen, Germany.Department of Pediatrics, Landes- Frauen- und Kinderklinik Linz, Linz, Austria.Department of Pediatrics, Bozen Hospital, Bozen, Italy.Department of Pediatrics, Graz Medical University, Graz, Austria.Department of Pediatric Neurology and Developmental Medicine, Dr von Hauner Children's Hospital, University of Munich, Munich, Germany.Department of Pediatrics, Klinikum rechts der Isar, Technische Universität, Munich, Germany.Pediatric Neurology, Department of Pediatrics, Klinikum Dritter Orden, Munich, Germany.Division of Pediatric Neurology, Department of Pediatrics, Klinikum Mutterhaus der Borromäerinnen, Trier, Germany.Radiological Institute, Kettenbrücke, Innsbruck, Austria.Department of Neuroradiology, Medical University of Innsbruck, Innsbruck, Austria Department of Neurology, Paracelsus Medical University of Salzburg, Salzburg, Austria.Clinical Department of Neurology, Innsbruck Medical University, Innsbruck, Austria.Clinical Department of Neurology, Innsbruck Medical University, Innsbruck, Austria.Division of Pediatric Neurology, Department of Pediatrics I, Innsbruck Medical University, Innsbruck, Austria.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25121570

Citation

Baumann, M, et al. "Clinical and Neuroradiological Differences of Paediatric Acute Disseminating Encephalomyelitis With and Without Antibodies to the Myelin Oligodendrocyte Glycoprotein." Journal of Neurology, Neurosurgery, and Psychiatry, vol. 86, no. 3, 2015, pp. 265-72.
Baumann M, Sahin K, Lechner C, et al. Clinical and neuroradiological differences of paediatric acute disseminating encephalomyelitis with and without antibodies to the myelin oligodendrocyte glycoprotein. J Neurol Neurosurg Psychiatry. 2015;86(3):265-72.
Baumann, M., Sahin, K., Lechner, C., Hennes, E. M., Schanda, K., Mader, S., Karenfort, M., Selch, C., Häusler, M., Eisenkölbl, A., Salandin, M., Gruber-Sedlmayr, U., Blaschek, A., Kraus, V., Leiz, S., Finsterwalder, J., Gotwald, T., Kuchukhidze, G., Berger, T., ... Rostásy, K. (2015). Clinical and neuroradiological differences of paediatric acute disseminating encephalomyelitis with and without antibodies to the myelin oligodendrocyte glycoprotein. Journal of Neurology, Neurosurgery, and Psychiatry, 86(3), 265-72. https://doi.org/10.1136/jnnp-2014-308346
Baumann M, et al. Clinical and Neuroradiological Differences of Paediatric Acute Disseminating Encephalomyelitis With and Without Antibodies to the Myelin Oligodendrocyte Glycoprotein. J Neurol Neurosurg Psychiatry. 2015;86(3):265-72. PubMed PMID: 25121570.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Clinical and neuroradiological differences of paediatric acute disseminating encephalomyelitis with and without antibodies to the myelin oligodendrocyte glycoprotein. AU - Baumann,M, AU - Sahin,K, AU - Lechner,C, AU - Hennes,E M, AU - Schanda,K, AU - Mader,S, AU - Karenfort,M, AU - Selch,C, AU - Häusler,M, AU - Eisenkölbl,A, AU - Salandin,M, AU - Gruber-Sedlmayr,U, AU - Blaschek,A, AU - Kraus,V, AU - Leiz,S, AU - Finsterwalder,J, AU - Gotwald,T, AU - Kuchukhidze,G, AU - Berger,T, AU - Reindl,M, AU - Rostásy,K, Y1 - 2014/08/13/ PY - 2014/8/15/entrez PY - 2014/8/15/pubmed PY - 2015/5/12/medline KW - MRI KW - NEUROIMMUNOLOGY KW - PAEDIATRIC NEUROLOGY SP - 265 EP - 72 JF - Journal of neurology, neurosurgery, and psychiatry JO - J. Neurol. Neurosurg. Psychiatry VL - 86 IS - 3 N2 - BACKGROUND: Myelin oligodendrocyte glycoprotein (MOG) antibodies have been recently described in children with acute disseminating encephalomyelitis (ADEM), but the clinical and neuroradiological characterisation of this subgroup is lacking. OBJECTIVE: To compare the clinical and neuroradiological features of paediatric ADEM with and without MOG antibodies. METHODS: Clinical course, cerebrospinal fluid (CSF)-, MRI studies, outcome and MOG status of 33 paediatric ADEM prospectively studied were reviewed. RESULTS: MOG antibodies (median 1:2560; range 1:160-1:20 480) were detected in 19 children with ADEM. The majority of children showed a decline of serum MOG-IgG titres over time. Children with MOG antibodies did not differ in their age at presentation, sex ratio, the presence of oligoclonal bands, clinical symptoms or initial severity, apart from a higher CSF cell count (p=0.038), compared with children without MOG antibodies. In addition, further relapsing demyelinating episodes associated with MOG antibodies were observed only in children with MOG antibodies. All 19 children with MOG antibodies had a uniform MRI pattern, characterised by large, hazy and bilateral lesions and the absence of atypical MRI features (eg, mainly small lesions, well-defined lesions), which was significantly different compared to that of children without MOG antibodies (p=0.003; and p=0.032, respectively). In addition, children with MOG antibodies had involvement of more anatomical areas (p=0.035) including the myelon characterised by a longitudinally extensive transverse myelitis (p=0.003), more often a complete resolution of lesions (p=0.036) and a better outcome (p=0.038). CONCLUSIONS: Patients with ADEM with MOG antibodies in our cohort had a uniform MRI characterised by large, bilateral and widespread lesions with an increased frequency of longitudinal extensive transverse myelitis and a favourable clinical outcome in contrast to children lacking MOG antibodies. SN - 1468-330X UR - https://www.unboundmedicine.com/medline/citation/25121570/Clinical_and_neuroradiological_differences_of_paediatric_acute_disseminating_encephalomyelitis_with_and_without_antibodies_to_the_myelin_oligodendrocyte_glycoprotein_ L2 - http://jnnp.bmj.com/cgi/pmidlookup?view=long&pmid=25121570 DB - PRIME DP - Unbound Medicine ER -