Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Observational Study
. 2023 Sep 26;101(13):e1376-e1381.
doi: 10.1212/WNL.0000000000207478. Epub 2023 Jun 19.

Timing and Predictors of T2-Lesion Resolution in Patients With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease

Laura Cacciaguerra  1 , Vyanka Redenbaugh  1 , John J Chen  1 , Pearse Morris  1 , Elia Sechi  1 , Stephanie B Syc-Mazurek  1 , A Sebastian Lopez-Chiriboga  1 , Jan-Mendelt Tillema  1 , Maria A Rocca  1 , Massimo Filippi  1 , Sean J Pittock  1 , Eoin P Flanagan  2
Affiliations
Observational Study

Timing and Predictors of T2-Lesion Resolution in Patients With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease

Laura Cacciaguerra et al. Neurology. .

Abstract

Objectives: To determine the timing and predictors of T2-lesion resolution in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).

Methods: This retrospective observational study using standard-of-care data had inclusion criteria of MOGAD diagnosis, ≥2 MRIs 12 months apart, and ≥1 brain/spinal cord T2-lesion. The median (interquartile range [IQR]) number of MRIs (82% at disease onset) per-patient were: brain, 5 (2-8); spine, 4 (2-8). Predictors of T2-lesion resolution were assessed with age- and sex-adjusted generalized estimating equations and stratified by T2-lesion size (small <1 cm; large ≥1 cm).

Results: We studied 583 T2-lesions (brain, 512 [88%]; spinal cord, 71 [12%]) from 55 patients. At last MRI (median follow-up 54 months [IQR 7-74]) 455 T2-lesions (78%) resolved. The median (IQR) time to resolution was 3 months (1.4-7.0). Small T2-lesions resolved more frequently and faster than large T2-lesions. Acute T1-hypointensity decreased the likelihood (odds ratio [95% CI]) of T2-lesion resolution independent of size (small: 0.23 [0.09-0.60], p = 0.002; large: 0.30 [0.16-0.55], p < 0.001), whereas acute steroids favored resolution of large T2-lesions (1.75 [1.01-3.03], p = 0.046). Notably, 32/55 (58%) T2-lesions resolved without treatment.

Discussion: The high frequency of spontaneous T2-lesion resolution suggests that this represents MOGAD's natural history. The speed of T2-lesion resolution and influence of size, corticosteroids, and T1-hypointensity on this phenomenon gives insight into MOGAD pathogenesis.

PubMed Disclaimer

Conflict of interest statement

L. Cacciaguerra received speaker and consultant honoraria from ACCMED, Roche, BMS Celgene, and Sanofi. V. Redenbaugh reports no disclosures. J.J. Chen served as consultant for Roche, Horizon, and UCB. P. Morris, E. Sechi, and S.B. Syc-Mazurek report no disclosures. A.S. Lopez-Chiriboga has served on advisory boards for Genentech and Horizon Therapeutics. J.-M. Tillema is associate editor for Journal of Child Neurology. M.A. Rocca received speaker honoraria from Bayer, Biogen, Bristol Myers Squibb, Celgene, Genzyme, Merck Serono, Novartis, Roche, and Teva, and receives research support from the MS Society of Canada and Fondazione Italiana Sclerosi Multipla. M. Filippi is editor-in-chief of the Journal of Neurology, associate editor of Human Brain Mapping, Radiology, and Neurological Sciences; received compensation for consulting services and/or speaking activities from Almiral, Alexion, Bayer, Biogen, Celgene, Eli Lilly, Genzyme, Merck-Serono, Novartis, Roche, Sanofi, Takeda, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Teva Pharmaceutical Industries, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA). S.J. Pittock reports grants, personal fees and nonfinancial support from Alexion Pharmaceuticals, Inc.; grants, personal fees, nonfinancial support and other support from MedImmune, Inc./Viela Bio, Inc.; personal fees for consulting from Genentech/Roche. He has a patent, Patent No. 8,889,102 (Application No. 12-678350, Neuromyelitis Optica Autoantibodies as a Marker for Neoplasia)—issued; a patent, Patent No. 9,891,219B2 (Application No. 12-573942, Methods for Treating Neuromyelitis Optica [NMO] by Administration of Eculizumab to an individual that is Aquaporin-4 [AQP4]-IgG Autoantibody positive)—issued. E.P. Flanagan has served on advisory boards for Alexion, Genentech and Horizon Therapeutics. He has received speaker honoraria from Pharmacy Times. He received royalties from UpToDate. E.P. Flanagan was a site primary investigator in a randomized clinical trial on Inebilizumab in neuromyelitis optica spectrum disorder run by Medimmune/Viela-Bio/Horizon Therapeutics. E.P. Flanagan has received funding from the NIH (R01NS113828). E.P. Flanagan is a member of the medical advisory board of the MOG project. E.P. Flanagan is an editorial board member of the Journal of the Neurological Sciences and Neuroimmunology Reports. A patent has been submitted on DACH1-IgG as a biomarker of paraneoplastic autoimmunity. Go to Neurology.org/N for full disclosures.

Figures

Figure 1
Figure 1. Examples of T2-Lesions Resolving or Persisting Over Time and in Different Locations in Patients With MOGAD
T2-lesions are shown on T2 fluid-attenuated inversion recovery in the brain and T2-weighted images in the spinal cord. Those T2-lesions persisting at the last follow-up are indicated by a white arrow. An example of early resolution with concomitant development of new lesions is shown in the first follow-up of the resolving lesions in the deep gray matter. m1–4 = follow-up acquired between 1 and 4 months from the baseline imaging; m12 = follow-up acquired at 12 months from the baseline imaging; MOGAD = myelin oligodendrocyte glycoprotein antibody–associated disease.
Figure 2
Figure 2. Forest Plot of Patient and Lesion Factors Associated With T2-Lesion Resolution in MOGAD
Bars correspond to odds ratio and 95% CIs derived from age- and sex-adjusted generalized estimating equations. The x-axis is in logarithmic scale to improve readability. For T2-lesion location, models were run separately for brain and spinal cord T2-lesions. Significant results are highlighted with * (red for negative associations and green for positive associations). The total number of T2-lesions presenting a certain feature and corresponding patients is also specified in the column on the right. #Odds ratio of T2-lesion resolution of T2-lesions <1 cm are missing in case of optic neuritis, brainstem syndrome, and diffusion restriction as none of the T2-lesions associated with optic neuritis resolved, and all T2-lesions observed during brainstem syndrome or with diffusion restriction resolved. ADEM = acute disseminated encephalomyelitis; EDSS = Expanded Disability Status Scale; IgG = immunoglobulin G; MOG = myelin oligodendrocyte glycoprotein; MOGAD = MOG antibody–associated disease.
See this image and copyright information in PMC

References

    1. Lopez-Chiriboga AS, Majed M, Fryer J, et al. . Association of MOG-IgG serostatus with relapse after acute disseminated encephalomyelitis and proposed diagnostic criteria for MOG-IgG-associated disorders. JAMA Neurol. 2018;75(11):1355-1363. doi:10.1001/jamaneurol.2018.1814 - DOI - PMC - PubMed
    1. Banks SA, Morris PP, Chen JJ, et al. . Brainstem and cerebellar involvement in MOG-IgG-associated disorder versus aquaporin-4-IgG and MS. J Neurol Neurosurg Psychiatry. 2020;92(4):384-390. doi:10.1136/jnnp-2020-325121 - DOI - PMC - PubMed
    1. Sechi E, Krecke KN, Messina SA, et al. . Comparison of MRI lesion evolution in different central nervous system demyelinating disorders. Neurology. 2021;97(11):e1097-e1109. doi:10.1212/wnl.0000000000012467 - DOI - PMC - PubMed
    1. Sechi E, Buciuc M, Pittock SJ, et al. . Positive predictive value of myelin oligodendrocyte glycoprotein Autoantibody testing. JAMA Neurol. 2021;78(6):741-746. doi:10.1001/jamaneurol.2021.0912 - DOI - PMC - PubMed
    1. Otani T, Irioka T, Igarashi S, Kaneko K, Takahashi T, Yokota T. Self-remitting cerebral cortical encephalitis associated with myelin oligodendrocyte glycoprotein antibody mimicking acute viral encephalitis: a case report. Mult Scler Relat Disord. 2020;41:102033. doi:10.1016/j.msard.2020.102033 - DOI - PubMed

Publication types

Substances