Clinical, Radiologic, and Prognostic Features of Myelitis Associated With Myelin Oligodendrocyte Glycoprotein Autoantibody.
Adolescent
Adult
Aged
Autoantibodies
/ immunology
Child
Child, Preschool
Encephalomyelitis, Acute Disseminated
/ diagnosis
Female
Humans
Immunoglobulin G
/ immunology
Male
Middle Aged
Myelin-Oligodendrocyte Glycoprotein
/ immunology
Myelitis, Transverse
/ diagnosis
Neoplasm Recurrence, Local
/ complications
Neuromyelitis Optica
/ diagnosis
Prognosis
Young Adult
Journal
JAMA neurology
ISSN: 2168-6157
Titre abrégé: JAMA Neurol
Pays: United States
ID NLM: 101589536
Informations de publication
Date de publication:
01 03 2019
01 03 2019
Historique:
pubmed:
24
12
2018
medline:
19
2
2020
entrez:
22
12
2018
Statut:
ppublish
Résumé
Recognizing the characteristics of myelin oligodendrocyte glycoprotein autoantibody (MOG-IgG) myelitis is essential for early accurate diagnosis and treatment. To evaluate the clinical, radiologic, and prognostic features of MOG-IgG myelitis and compare with myelitis with aquaporin-4-IgG (AQP4-IgG) and multiple sclerosis (MS). We retrospectively identified 199 MOG-IgG-positive Mayo Clinic patients from January 1, 2000, through December 31, 2017, through our neuroimmunology laboratory. Fifty-four patients met inclusion criteria of (1) clinical myelitis; (2) MOG-IgG positivity; and (3) medical records available. We excluded 145 patients without documented myelitis. Myelitis of AQP4-IgG (n = 46) and MS (n = 26) were used for comparison. Outcome variables included modified Rankin score and need for gait aid. A neuroradiologist analyzed spine magnetic resonance imaging of patients with MOG-IgG and control patients blinded to diagnosis. Of 54 included patients with MOG-IgG myelitis, the median age was 25 years (range, 3-73 years) and 24 were women (44%). Isolated transverse myelitis was the initial manifestation in 29 patients (54%), and 10 (19%) were initially diagnosed as having viral/postviral acute flaccid myelitis. Cerebrospinal fluid-elevated oligoclonal bands occurred in 1 of 38 (3%). At final follow-up (median, 24 months; range, 2-120 months), 32 patients (59%) had developed 1 or more relapses of optic neuritis (n = 31); transverse myelitis (n = 7); or acute disseminated encephalomyelitis (n = 1). Clinical features favoring MOG-IgG myelitis vs AQP4-IgG or MS myelitis included prodromal symptoms and concurrent acute disseminated encephalomyelitis. Magnetic resonance imaging features favoring MOG-IgG over AQP4-IgG or MS myelitis were T2-signal abnormality confined to gray matter (sagittal line and axial H sign) and lack of enhancement. Longitudinally extensive T2 lesions were of similar frequency in MOG-IgG and AQP4-IgG myelitis (37 of 47 [79%] vs 28 of 34 [82%]; P = .52) but not found in MS. Multiple spinal cord lesions and conus involvement were more frequent with MOG-IgG than AQP4-IgG but not different from MS. Wheelchair dependence at myelitis nadir occurred in one-third of patients with MOG-IgG and AQP4-IgG but never with MS, although patients with MOG-IgG myelitis recovered better than those with AQP4-IgG. Myelitis is an early manifestation of MOG-IgG-related disease and may have a clinical phenotype of acute flaccid myelitis. We identified a variety of clinical and magnetic resonance imaging features that may help clinicians identify those at risk in whom MOG-IgG should be tested.
Identifiants
pubmed: 30575890
pii: 2719280
doi: 10.1001/jamaneurol.2018.4053
pmc: PMC6440233
doi:
Substances chimiques
Autoantibodies
0
Immunoglobulin G
0
Myelin-Oligodendrocyte Glycoprotein
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
301-309Subventions
Organisme : NCATS NIH HHS
ID : UL1 TR002535
Pays : United States
Références
Ann Neurol. 2016 Mar;79(3):437-47
pubmed: 26677112
Continuum (Minneap Minn). 2011 Aug;17(4):733-43
pubmed: 22810928
Brain. 2017 Dec 1;140(12):3128-3138
pubmed: 29136091
J Neurol Neurosurg Psychiatry. 2017 Mar;88(3):218-225
pubmed: 27913626
JAMA Neurol. 2015 Jan;72(1):81-7
pubmed: 25384099
Lancet Neurol. 2016 Apr;15(4):391-404
pubmed: 26906964
Nat Neurosci. 2013 May;16(5):571-9
pubmed: 23542689
Neurology. 2017 Jul 11;89(2):129-137
pubmed: 28615421
Brain. 2017 Mar 1;140(3):617-627
pubmed: 28364548
Ann Neurol. 2016 Sep;80(3):326-38
pubmed: 27422805
Neurology. 2013 Oct 1;81(14):1197-204
pubmed: 23997151
PLoS One. 2013 Oct 23;8(10):e78480
pubmed: 24194939
J Neurol. 2017 Sep;264(9):1945-1955
pubmed: 28770374
J Neurol Neurosurg Psychiatry. 2004 Oct;75(10):1431-5
pubmed: 15377691
J Neurol Sci. 2017 Oct 15;381:240-244
pubmed: 28991690
Neurology. 2015 Jul 14;85(2):177-89
pubmed: 26092914
Ann Neurol. 2006 Mar;59(3):566-9
pubmed: 16453327
Neurology. 2018 Jan 9;90(2):e96-e102
pubmed: 29247071
Lancet. 2015 Apr 25;385(9978):1662-71
pubmed: 25638662
Ophthalmology. 2018 Oct;125(10):1628-1637
pubmed: 29716788
Nat Rev Neurol. 2013 Aug;9(8):455-61
pubmed: 23797245
Neurology. 2017 Aug 29;89(9):900-908
pubmed: 28768844
J Neurol Neurosurg Psychiatry. 2017 Oct;88(10):811-817
pubmed: 28684532
Neurology. 2012 Sep 18;79(12):1273-7
pubmed: 22914827
J Neurol Neurosurg Psychiatry. 2018 Feb;89(2):118
pubmed: 29175896
Ann Neurol. 2016 May;79(5):775-783
pubmed: 26891082
JAMA Neurol. 2018 Nov 1;75(11):1355-1363
pubmed: 30014148
J Exp Med. 2005 Aug 15;202(4):473-7
pubmed: 16087714
Neurology. 2007 Apr 17;68(16 Suppl 2):S7-12
pubmed: 17438241
J Neuroinflammation. 2018 May 3;15(1):134
pubmed: 29724224
J Neurol Neurosurg Psychiatry. 2013 Aug;84(8):909-14
pubmed: 23431079
Proc Natl Acad Sci U S A. 2009 May 19;106(20):8083-4
pubmed: 19451620
Brain. 2005 Aug;128(Pt 8):1877-86
pubmed: 15901645
Ann Indian Acad Neurol. 2014 Jan;17(1):85-8
pubmed: 24753667
J Neuroinflammation. 2016 Sep 27;13(1):280
pubmed: 27793206
J Neurol Neurosurg Psychiatry. 2018 Feb;89(2):127-137
pubmed: 29142145