Nat Immunol. developed a cell-based assay using Reports about prevalence of anti-MOG in selected Multiple Sclerosis cases began to appear in 2016Inflammatory demyelinating disease previously considered part of the multiple sclerosis spectrumJarius S, Metz I, König FB, Ruprecht K, Reindl M, Paul F, Brück W, Wildemann B.
It has been classified inside the anti-MOG associated inflammatory demyelinating diseases.
BMC Neurol. Epub 2014 Aug 13.Fukushima N, Suzuki M, Ogawa R, Hayashi K, Takanashi JI, Ohashi T.Rinsho Shinkeigaku.
Epstein-Barr virus infections of the nervous system. MOG-AD is an inflammatory demyelinating condition of the CNS characterised by a monophasic or relapsing course of neurological dysfunction, which does not meet the typical criteria for MS or other known neuroinflammatory conditions and occurs in the presence of serum MOG antibodies detected using specific cell-based assays [].Although in most cases demyelination associated with MOG … Cell-based immunoassays revealed positivity for anti-MOG antibody with a titer of 1:1024 and negativity for anti-aquaporin-4 antibody.
Anti-MOG autoimmunity has been found to be involved in the seronegative NMO and also in optic neuritis and some fulminant forms of ADEM MOG antibodies in NMOSD are variable depending on the seropositivity status. Handb Clin Neurol. Epub 2017 Aug 31.Vakrakou AG, Tzanetakos D, Argyrakos T, Koutsis G, Evangelopoulos ME, Andreadou E, Anagnostouli M, Breza M, Tzartos JS, Gialafos E, Dimitrakopoulos AN, Velonakis G, Toulas P, Stefanis L, Kilidireas C.Front Neurol. 2007;68(16 Suppl 2):S23–36.Baumann M, Sahin K, Lechner C, Hennes EM, Schanda K, Mader S, et al. In many kids, the MOG antibody disappears within 1 year and relapses do not occur. In some, the MOG antibody persists and relapses may occur.
Key Points.
Volume 120, May 2019, Pages 66-73, doi: Deena A. Tajfirouz, M. Tariq Bhatti, John J. Chen, Clinical Characteristics and Treatment of MOG-IgG–Associated Optic Neuritis
1994;307:45–8.Junker AK, Roland EH, Hahn G. Transverse myelitis and Epstein-Barr virus infection with delayed antibody responses. The clinical presentation is variable and largely dependent upon the overall clinical manifestation. The heralding and-or major manifestation. Laboratory analysis showed elevated white blood count (10,390/mmSpinal cord T2-weighted MRI shows a hyperintense lesion extending from C2 to C6 on the sagittal view (We present a case of a patient who developed anti-MOG antibody-positive ADEM following IM.
Jarius et al.
2020 Jun 30;11:536. doi: 10.3389/fneur.2020.00536. A post-infectious autoimmune process has been proposed as a possible pathophysiologic mechanism.Demyelinating lesions of MOG-associated encephalomyelitis resemble more those observed in Serum live cell-based assays are the gold standard for anti-MOG antibody testing. Oshiro A, Nakamura S, Tamashiro K, Fujihara K. Anti-MOG + neuromyelitis optica spectrum disorders treated with plasmapheresis, No To Hattatsu. Influenza-associated MOG antibody-positive longitudinally extensive transverse myelitis: a case report. Aquaporin 4 antibodies were detected in 1 participant, who was negative for anti-MOG antibodies.
The present case illustrates two important clinical issues.
In comparison to the larger number of pediatric cases with acquired demyelinating diseases associated with MOG antibodies, adult cases with NMO or opticospinal MS are rare, and some recent studies provided clear evidence that MOG antibody–positive ADEM cases have clinical presentations resembling NMO (e.g., LETM and recurrent ON). This study suggests that anti-MOG antibodies can be … All authors approved the contents of this case report.The authors declare that they have no competing interests.Written informed consent was obtained from the patient for publication of this case report and any accompanying images.The authors declare that ethics approval was not required for this case report.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.Division of Neurology, Department of Internal Medicine IV, Osaka Medical College, Daigakumachi 2-7, Takatsukishi, Osaka, 569-8686, JapanYoshitsugu Nakamura, Hideto Nakajima, Hiroki Tani, Takafumi Hosokawa, Shimon Ishida & Fumiharu KimuraDivision of Neurology, Tohoku University School of Medicine, Seiryomachi 1-1, Aobaku, Sendai, 980-8574, JapanDivision of Neurology, NHO Yonezawa Hospital, Ozimisawa 26100-1, Yonezawashi, Yamagata, 992-1202, JapanYou can also search for this author in
In other conditions.
In this review, we discuss MOG-positive cases presenting with encephalitis, encephalopathy, or ADEM-like presentation based on recently published series.
Acute disseminated encephalomyelitis.
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