Bahadır Konuskan1, Mirac Yildirim2, Rahsan Gocmen3, Tuncay Derya Okur4, Ipek Polat4, Huseyin Kilic5, Sema Saltik6, Zeynep Ozturk7, Kivilcim Gucuyener8, Sakir Altunbasak9, Tamer Celik10, Gulsen Kose11, Arzu Yilmaz12, Mustafa Komur13, Hulya Kayilioglu14, Banu Anlar15. 1. Department of Pediatric Neurology, Hacettepe University Ihsan Dogramaci Children's Hospital, Ankara, Turkey. 2. Department of Pediatric Neurology, Konya Research and Training Hospital, Konya, Turkey. Electronic address: miracyildirim81@hotmail.com. 3. Department of Radiology, Hacettepe University Hospitals, Ankara, Turkey. 4. Department of Pediatric Neurology, Dokuz Eylul University Hospital, Izmir, Turkey. 5. Department of Pediatric Neurology, Istanbul University Cerrahpasa School of Medicine Hospital, Istanbul, Turkey. Electronic address: kilichuseyin@me.com. 6. Department of Pediatric Neurology, Istanbul University Cerrahpasa School of Medicine Hospital, Istanbul, Turkey. Electronic address: semasaltik@superonline.com. 7. Department of Pediatric Neurology, Gazi University Hospital, Ankara, Turkey. 8. Department of Pediatric Neurology, Gazi University Hospital, Ankara, Turkey. Electronic address: kivilcim@gazi.edu.tr. 9. Department of Pediatric Neurology, Cukurova University Hospital, Adana, Turkey. 10. Department of Pediatric Neurology, Adana Numune Research and Training Hospital, Adana, Turkey. 11. Department of Pediatric Neurology, Sisli Hamidiye Etfal Research and Training Hospital, Istanbul, Turkey. 12. Department of Pediatric Neurology, Ankara Research and Training Hospital, Ankara, Turkey. 13. Department of Pediatric Neurology, Mersin University Hospital, Mersin, Turkey. 14. Department of Pediatric Neurology, Dr. Sami Ulus Research and Training Hospital, Ankara, Turkey. 15. Department of Pediatric Neurology, Hacettepe University Ihsan Dogramaci Children's Hospital, Ankara, Turkey. Electronic address: banlar@hacettepe.edu.tr.
Abstract
BACKGROUND: Knowledge has been expanding on myelin oligodendrocyte glycoprotein (MOG) antibody-associated central nervous system disorders. We delineate the clinical and paraclinical findings and outcome of our pediatric patients with MOG antibody seropositive disease. METHODS: We retrospectively analyzed the clinical presentation, cerebrospinal fluid findings, magnetic resonance imaging (MRI) studies, course and outcome of children seropositive for anti-MOG IgG. RESULTS: Total 20 children with neurological symptoms and serum anti-MOG IgG were identified from six centers in Turkey. Median age at onset was 9 years (mean 8.8 ± 5.0 years, range: 1.5-16.5 years). Final diagnoses were acute disseminated encephalomyelitis (ADEM) (n = 5), ADEM + optic neuritis (n = 4), neuromyelitis optica spectrum disorder (NMOSD) (n = 3), myelitis (n = 2), relapsing optic neuritis (n = 2), multiphasic DEM (n = 3), and unclassified relapsing demyelinating disease (n = 1). Seven/20 (35%) children experienced a single episode while 13/20 (65%) had a least one relapse during follow-up. On MRI, subcortical white matter, brainstem, and corpus callosum were preferentially involved regions. Full recovery was observed in 15/20 (75%) children. CONCLUSION: MOG autoimmunity in children has a wide clinical spectrum, tendency to relapse, and a favourable outcome compared with other relapsing demyelinating diseases.
BACKGROUND: Knowledge has been expanding on myelin oligodendrocyte glycoprotein (MOG) antibody-associated central nervous system disorders. We delineate the clinical and paraclinical findings and outcome of our pediatric patients with MOG antibody seropositive disease. METHODS: We retrospectively analyzed the clinical presentation, cerebrospinal fluid findings, magnetic resonance imaging (MRI) studies, course and outcome of children seropositive for anti-MOG IgG. RESULTS: Total 20 children with neurological symptoms and serum anti-MOG IgG were identified from six centers in Turkey. Median age at onset was 9 years (mean 8.8 ± 5.0 years, range: 1.5-16.5 years). Final diagnoses were acute disseminated encephalomyelitis (ADEM) (n = 5), ADEM + optic neuritis (n = 4), neuromyelitis optica spectrum disorder (NMOSD) (n = 3), myelitis (n = 2), relapsing optic neuritis (n = 2), multiphasic DEM (n = 3), and unclassified relapsing demyelinating disease (n = 1). Seven/20 (35%) children experienced a single episode while 13/20 (65%) had a least one relapse during follow-up. On MRI, subcortical white matter, brainstem, and corpus callosum were preferentially involved regions. Full recovery was observed in 15/20 (75%) children. CONCLUSION:MOGautoimmunity in children has a wide clinical spectrum, tendency to relapse, and a favourable outcome compared with other relapsing demyelinating diseases.