MOG encephalomyelitis: distinct clinical, MRI and CSF features in patients with longitudinal extensive transverse myelitis as first clinical presentation.
Diagnosis
Longitudinal extensive transverse myelitis (LETM)
Myelin oligodendrocyte glycoprotein (MOG) antibodies
Myelitis
Neuromyelitis optica spectrum disorders (NMOSD)
Journal
Journal of neurology
ISSN: 1432-1459
Titre abrégé: J Neurol
Pays: Germany
ID NLM: 0423161
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
received:
18
12
2019
accepted:
08
02
2020
revised:
06
02
2020
pubmed:
15
2
2020
medline:
18
3
2021
entrez:
15
2
2020
Statut:
ppublish
Résumé
Based on clinical, immunological and histopathological evidence, MOG-IgG-associated encephalomyelitis (MOG-EM) has emerged as a distinct disease entity different from multiple sclerosis (MS) and aquaporin-4-antibody-positive neuromyelitis optica spectrum disorder (NMOSD). MOG-EM is associated with a broader clinical phenotype including optic neuritis, myelitis, brainstem lesions and acute disseminated encephalomyelitis with a substantial clinical and radiological overlap to other demyelinating CNS disorders. To evaluate common clinical, MRI and CSF findings, as well as therapy responses in patients with longitudinal extensive transverse myelitis (LETM) as initial clinical presentation of MOG-EM. After excluding patients with a known diagnosis of MS, we identified 153 patients with myelitis of which 7 fulfilled the inclusion criteria and were investigated for MRI, CSF and clinical parameters. Patients with LETM as first clinical presentation of MOG-EM display similar characteristics, namely a lack of gadolinium-enhancement in spinal cord MRI, marked pleocytosis, negative oligoclonal bands, a previous history of infections/vaccinations and response to antibody-depleting treatments for acute attacks and long-term treatment. We identify common pathological findings in patients with LETM as first clinical presentation of MOG-EM which distinguishes it from other forms of LETM and should lead to testing for MOG-IgG in these cases.
Sections du résumé
BACKGROUND
BACKGROUND
Based on clinical, immunological and histopathological evidence, MOG-IgG-associated encephalomyelitis (MOG-EM) has emerged as a distinct disease entity different from multiple sclerosis (MS) and aquaporin-4-antibody-positive neuromyelitis optica spectrum disorder (NMOSD). MOG-EM is associated with a broader clinical phenotype including optic neuritis, myelitis, brainstem lesions and acute disseminated encephalomyelitis with a substantial clinical and radiological overlap to other demyelinating CNS disorders.
OBJECTIVE
OBJECTIVE
To evaluate common clinical, MRI and CSF findings, as well as therapy responses in patients with longitudinal extensive transverse myelitis (LETM) as initial clinical presentation of MOG-EM.
METHODS
METHODS
After excluding patients with a known diagnosis of MS, we identified 153 patients with myelitis of which 7 fulfilled the inclusion criteria and were investigated for MRI, CSF and clinical parameters.
RESULTS
RESULTS
Patients with LETM as first clinical presentation of MOG-EM display similar characteristics, namely a lack of gadolinium-enhancement in spinal cord MRI, marked pleocytosis, negative oligoclonal bands, a previous history of infections/vaccinations and response to antibody-depleting treatments for acute attacks and long-term treatment.
CONCLUSIONS
CONCLUSIONS
We identify common pathological findings in patients with LETM as first clinical presentation of MOG-EM which distinguishes it from other forms of LETM and should lead to testing for MOG-IgG in these cases.
Identifiants
pubmed: 32055995
doi: 10.1007/s00415-020-09755-x
pii: 10.1007/s00415-020-09755-x
pmc: PMC7293681
doi:
Substances chimiques
Autoantibodies
0
MOG protein, human
0
Myelin-Oligodendrocyte Glycoprotein
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1632-1642Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : CRC-TR-128
Organisme : Gemeinnützige Hertie-Stiftung
ID : myLab17
Références
Reindl M, Waters P (2019) Myelin oligodendrocyte glycoprotein antibodies in neurological disease. Nat Rev Neurol 15(2):89–102
doi: 10.1038/s41582-018-0112-x
Jarius S, Paul F, Aktas O, Asgari N, Dale RC, de Seze J et al (2018) MOG encephalomyelitis: international recommendations on diagnosis and antibody testing. J Neuroinflamm 15(1):134
doi: 10.1186/s12974-018-1144-2
Weber MS, Derfuss T, Bruck W (2018) Anti-myelin oligodendrocyte glycoprotein antibody-associated central nervous system demyelination-a novel disease entity? JAMA Neurol 75(8):909–910
doi: 10.1001/jamaneurol.2018.1055
Dos Passos GR, Oliveira LM, da Costa BK, -Pereira SL, Callegaro D, Fujihara K et al (2018) MOG-IgG-associated optic neuritis, encephalitis, and myelitis: lessons learned from neuromyelitis optica spectrum disorder. Front Neurol 9:217
doi: 10.3389/fneur.2018.00217
van Pelt ED, Wong YY, Ketelslegers IA, Hamann D, Hintzen RQ (2016) Neuromyelitis optica spectrum disorders: comparison of clinical and magnetic resonance imaging characteristics of AQP4-IgG versus MOG-IgG seropositive cases in the Netherlands. Eur J Neurol 23(3):580–587
doi: 10.1111/ene.12898
McLaughlin KA, Chitnis T, Newcombe J, Franz B, Kennedy J, McArdel S et al (2009) Age-dependent B cell autoimmunity to a myelin surface antigen in pediatric multiple sclerosis. J Immunol 183(6):4067–4076
doi: 10.4049/jimmunol.0801888
Probstel AK, Dornmair K, Bittner R, Sperl P, Jenne D, Magalhaes S et al (2011) Antibodies to MOG are transient in childhood acute disseminated encephalomyelitis. Neurology 77(6):580–588
doi: 10.1212/WNL.0b013e318228c0b1
Ramanathan S, Mohammad S, Tantsis E, Nguyen TK, Merheb V, Fung VSC et al (2018) Clinical course, therapeutic responses and outcomes in relapsing MOG antibody-associated demyelination. J Neurol Neurosurg Psychiatry 89(2):127–137
doi: 10.1136/jnnp-2017-316880
Hennes EM, Baumann M, Lechner C, Rostasy K (2018) MOG Spectrum Disorders and Role of MOG-Antibodies in Clinical Practice. Neuropediatrics 49(1):3–11
doi: 10.1055/s-0037-1604404
Cobo-Calvo A, Ruiz A, D'Indy H, Poulat AL, Carneiro M, Philippe N et al (2017) MOG antibody-related disorders: common features and uncommon presentations. J Neurol 264(9):1945–1955
doi: 10.1007/s00415-017-8583-z
Pandit L, Sato DK, Mustafa S, Takahashi T, D'Cunha A, Malli C et al (2016) Relapsing optic neuritis and isolated transverse myelitis are the predominant clinical phenotypes for patients with antibodies to myelin oligodendrocyte glycoprotein in India. Multiple Scler J Exp Transl Clin 2:2055217316675634
Cobo-Calvo A, Ruiz A, Maillart E, Audoin B, Zephir H, Bourre B et al (2018) Clinical spectrum and prognostic value of CNS MOG autoimmunity in adults: The MOGADOR study. Neurology 90(21):e1858–e1869
doi: 10.1212/WNL.0000000000005560
Dubey D, Pittock SJ, Krecke KN, Morris PP, Sechi E, Zalewski NL et al (2019) Clinical, radiologic, and prognostic features of myelitis associated with myelin oligodendrocyte glycoprotein autoantibody. JAMA Neurol 76(3):301–309
doi: 10.1001/jamaneurol.2018.4053
Sechi E, Shosha E, Williams JP, Pittock SJ, Weinshenker BG, Keegan BM et al (2019) Aquaporin-4 and MOG autoantibody discovery in idiopathic transverse myelitis epidemiology. Neurology 93(4):e414–e420
doi: 10.1212/WNL.0000000000007828
Tantsis EM, Prelog K, Alper G, Benson L, Gorman M, Lim M et al (2019) Magnetic resonance imaging in enterovirus-71, myelin oligodendrocyte glycoprotein antibody, aquaporin-4 antibody, and multiple sclerosis-associated myelitis in children. Dev Med Child Neurol 61(9):1108–1116
doi: 10.1111/dmcn.14114
Jarius S, Ruprecht K, Kleiter I, Borisow N, Asgari N, Pitarokoili K et al (2016) MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome. J Neuroinflamm 13(1):280
Trebst C, Raab P, Voss EV, Rommer P, Mugheisib M, Zettl UK et al (2011) Longitudinal extensive transverse myelitis–it's not all neuromyelitis optica. Nat Rev Neurol 7(12):688–698
doi: 10.1038/nrneurol.2011.176
Thompson AJ, Banwell BL, Barkhof F, Carroll WM, Coetzee T, Comi G et al (2018) Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol 17(2):162–173
doi: 10.1016/S1474-4422(17)30470-2
Flanagan EP, Kaufmann TJ, Krecke KN, Aksamit AJ, Pittock SJ, Keegan BM et al (2016) Discriminating long myelitis of neuromyelitis optica from sarcoidosis. Ann Neurol 79(3):437–447
doi: 10.1002/ana.24582
Asgari N, Flanagan EP, Fujihara K, Kim HJ, Skejoe HP, Wuerfel J et al (2017) Disruption of the leptomeningeal blood barrier in neuromyelitis optica spectrum disorder. Neurol Neuroimmunol Neuroinflamm 4(4):e343
Wingerchuk DM, Banwell B, Bennett JL, Cabre P, Carroll W, Chitnis T et al (2015) International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology 85(2):177–189
doi: 10.1212/WNL.0000000000001729
Wingerchuk DM, Lennon VA, Pittock SJ, Lucchinetti CF, Weinshenker BG (2006) Revised diagnostic criteria for neuromyelitis optica. Neurology 66(10):1485–1489
doi: 10.1212/01.wnl.0000216139.44259.74
Jarius S, Ruprecht K, Kleiter I, Borisow N, Asgari N, Pitarokoili K et al (2016) MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 1: Frequency, syndrome specificity, influence of disease activity, long-term course, association with AQP4-IgG, and origin. J Neuroinflamm 13(1):279
Franciotta D, Cabezas S, Andreoni L, Ravaglia S, Jarius S, Romagnolo S et al (2008) Oligoclonal IgG band patterns in inflammatory demyelinating human and mouse diseases. J Neuroimmunol 200(1–2):125–128
doi: 10.1016/j.jneuroim.2008.06.004
Jarius S, Paul F, Franciotta D, Ruprecht K, Ringelstein M, Bergamaschi R et al (2011) Cerebrospinal fluid findings in aquaporin-4 antibody positive neuromyelitis optica: results from 211 lumbar punctures. J Neurol Sci 306(1–2):82–90
doi: 10.1016/j.jns.2011.03.038
Narayan R, Simpson A, Fritsche K, Salama S, Pardo S, Mealy M et al (2018) MOG antibody disease: A review of MOG antibody seropositive neuromyelitis optica spectrum disorder. Multiple Scler Relat Disord 25:66–72
doi: 10.1016/j.msard.2018.07.025
Tea F, Lopez JA, Ramanathan S, Merheb V, Lee FXZ, Zou A et al (2019) Characterization of the human myelin oligodendrocyte glycoprotein antibody response in demyelination. Acta Neuropathol Commun 7(1):145
doi: 10.1186/s40478-019-0786-3
Waters P, Vincent A (2019) Myelin oligodendrocyte glycoprotein CSF testing needs testing. Neurology 93(20):871–872
pubmed: 31645474
Di Pauli F, Mader S, Rostasy K, Schanda K, Kornek B, Ehling R et al (2011) Temporal dynamics of anti-MOG antibodies in CNS demyelinating diseases. Clin Immunol (Orlando, Fla) 138(3):247–254
doi: 10.1016/j.clim.2010.11.013
Hoftberger R, Sepulveda M, Armangue T, Blanco Y, Rostasy K, Calvo AC et al (2015) Antibodies to MOG and AQP4 in adults with neuromyelitis optica and suspected limited forms of the disease. Multiple Scler (Houndmills, Basingstoke, England) 21(7):866–874
doi: 10.1177/1352458514555785
Oliveira LM, -Pereira SL, Pitombeira MS, Torretta PH, Callegaro D, Sato DK (2019) Persistent MOG-IgG positivity is a predictor of recurrence in MOG-IgG-associated optic neuritis, encephalitis and myelitis. Multiple Scler (Houndmills, Basingstoke, England) 25(14):1907–1914
doi: 10.1177/1352458518811597
Kitley J, Woodhall M, Waters P, Leite MI, Devenney E, Craig J et al (2012) Myelin-oligodendrocyte glycoprotein antibodies in adults with a neuromyelitis optica phenotype. Neurology 79(12):1273–1277
doi: 10.1212/WNL.0b013e31826aac4e
Kitley J, Waters P, Woodhall M, Leite MI, Murchison A, George J et al (2014) Neuromyelitis optica spectrum disorders with aquaporin-4 and myelin-oligodendrocyte glycoprotein antibodies: a comparative study. JAMA Neurol 71(3):276–283
doi: 10.1001/jamaneurol.2013.5857
Sato DK, Callegaro D, Peixoto MA, Waters PJ, de Jorge FM, Takahashi T et al (2014) Distinction between MOG antibody-positive and AQP4 antibody-positive NMO spectrum disorders. Neurology 82(6):474–481
doi: 10.1212/WNL.0000000000000101