Anti-MOG associated encephalomyelitis

Anti-MOG associated encephalomyelitis is an inflammatory demyelinating disease of the central nervous system. Serum anti-myelin oligodendrocyte glycoprotein antibodies are present in up to half of patients with an acquired demyelinating syndrome and have been described in association with a range of phenotypic presentations, including acute disseminated encephalomyelitis, optic neuritis, and transverse myelitis[1].

Presentation

The clinical presentation is variable and largely dependent upon the overall clinical manifestation.

The presence of anti-MOG autoantibodies has been described in association with the following conditions:[2]

Some of them have been studied in detail:

Seronegative neuromyelitis optica

Anti-MOG antibodies have been described in some patients with NMOSD[10][11] who were negative for the aquaporin 4 (AQP-4) antibody. However, NMOSD is an astrocytopathy, whereas MOG antibody-associated disease is an oligodendrocytopathy, suggesting that these are two separate pathologic entities[12]. Rare cases have been described of patients with antibodies against both AQP4 and MOG. These patients typically have MS-like brain lesions, multifocal spine lesions and optic nerve atrophy[13]. However, the coexistence of both antibodies is still a matter of ongoing debate[14].

ADEM

The presence of anti-MOG antibodies is more common in children with ADEM[15].

Tumefactive demyelination

Rare cases of anti-MOG antibodies in association with tumefactive multiple sclerosis have been described[16].

Causes

The etiology of anti-MOG disease remains unknown, but a post-infectious autoimmune process has been proposed as a possible pathophysiologic mechanism[17]. Other reports point to molecular mimicry between MOG and some viruses as a possible etiology[18].

Histopathology

Demyelinating lesions of MOG-associated encephalomyelitis resemble more those observed in multiple sclerosis[19] than NMO. They are similar to pattern-II multiple sclerosis[20] with T-cells and macrophages surrounding blood vessels, preservation of oligodendrocytes and signs of complement system activation.

Diagnosis

Serum live cell-based assays are the gold standard for anti-MOG antibody testing. Cerebrospinal fluid analysis is less sensitive and specific compared to serum testing[21]. Cerebrospinal fluid oligoclonal bands are uncommon.

Proposed diagnostic criteria require serum positivity for MOG antibody, a clinical presentation consistent with an acquired demyelinating syndrome, and exclusion of an alternative diagnosis[22].

In the young, MRI typically shows ADEM–like lesions and longitudinally extensive transverse myelitis (LETM), whereas optic neuritis and short transverse myelitis are more commonly seen in older patients[23]. However, rare cases of symptomatic MRI-negative MOG-related disease have been described[24].

Clinical course

Two clinical courses have been described:[25]

  • Monophasic (most common)
  • Relapsing

Prognosis

Residual disability develops in 50–80% of patients, with transverse myelitis at onset being the most significant predictor of long-term outcome.

Treatment

Acute therapy consists of high-dose corticosteroids, IVIG, or plasma exchange, and long-term immunosuppression may be necessary in recurrent cases.[26][27]. Anti-MOG positive patients should not be treated with interferons as these may worsen the disease course similar to those with NMOSD[21]. There are also anecdotal reports against using fingolimod.[28].

Research

Animal models in experimental autoimmune encephalomyelitis, EAE, have shown that “MOG-specific EAE models (of different animal strains) display/mirror human multiple sclerosis" but EAE pathology is closer to NMO and ADEM than to the confluent demyelination observed in MS.[29].

History

Reports describing the possible involvement of anti-MOG antibodies in multiple sclerosis and other demyelinating conditions first appeared in the literature in the late 1980s, but evidence to support their role in demyelinating disease was always weak and inconsistent[30]. The turning point was in 2011, when Mader et al. developed a cell-based assay using HEK 293 cells which increased the detection rate of these antibodies in the serum[31].

References

  1. Sudarshini Ramanathan, Russell C. Dale, Fabienne Brilot, Anti-MOG antibody: The history, clinical phenotype, and pathogenicity of a serum biomarker for demyelination. Autoimmunity Reviews, Volume 15, Issue 4, April 2016, Pages 307–324, doi:10.1016/j.autrev.2015.12.004
  2. Reindl, M; Di Pauli, F; Rostásy, K; Berger, T (Aug 2013). "The spectrum of MOG autoantibody-associated demyelinating diseases". Nat Rev Neurol. 9 (8): 455–61. doi:10.1038/nrneurol.2013.118. PMID 23797245.
  3. Jae-Won Hyun el al. Longitudinal analysis of myelin oligodendrocyte glycoprotein antibodies in CNS inflammatory diseases, doi: https://dx.doi.org/10.1136/jnnp-2017-315998
  4. Baumann, M.; Hennes, E.M.; Schanda, K.; Karenfort, M.; Bajer-Kornek, B.; Diepold, K.; Fiedler, B.; Marquardt, I.; Strautmanis, J.; Vieker, S.; Reindl, M.; Rostásy, K. (2015). "Clinical characteristics and neuroradiological findings in children with multiphasic demyelinating encephalomyelitis and MOG antibodies". European Journal of Paediatric Neurology. 19 (Supplement 1): S21. doi:10.1016/S1090-3798(15)30066-0.
  5. Jarius S, Metz I, König FB, Ruprecht K, Reindl M, Paul F, Brück W, Wildemann B. "Screening for MOG-IgG and 27 other anti-glial and anti-neuronal autoantibodies in 'pattern II multiple sclerosis' and brain biopsy findings in a MOG-IgG-positive case Mult Scler. 2016 Feb;
  6. Franziska Di Pauli, Romana Höftberger, Markus Reindl, Ronny Beer, Paul Rhomberg, Kathrin Schanda, Douglas Sato, Kazuo Fujihara, Hans Lassmann, Erich Schmutzhard and Thomas Berger, Fulminant demyelinating encephalomyelitis. Insights from antibody studies and neuropathology. Neurol Neuroimmunol Neuroinflamm December 2015 vol. 2 no. 6 e175. doi=https://dx.doi.org/10.1212/NXI.0000000000000175
  7. Melania Spadaro et al., Autoantibodies to MOG in a distinct subgroup of adult multiple sclerosis, Neurol Neuroimmunol Neuroinflamm, October 2016 vol. 3 no. 5 e257, doi:10.1212/NXI.0000000000000257
  8. Chalmoukou, Konstantina; et al. (2015). "Anti-MOG antibodies are frequently associated with steroid-sensitive recurrent optic neuritis". Neurol Neuroimmunol Neuroinflamm. 2 (4): e131. doi:10.1212/NXI.0000000000000131. PMC 4496630. PMID 26185777.
  9. Ram N Narayan Cynthia Wang Peter Sguigna Khalil Husari Benjamin Greenberg, Atypical Anti-MOG syndrome with aseptic meningoencephalitis and pseudotumor cerebri-like presentations, Multiple Sclerosis and Related Disorders, Volume 27, January 2019, Pages 30-33, https://doi.org/10.1016/j.msard.2018.10.003
  10. Pröbstel, Anne-Katrin; et al. (2015). "Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype". Journal of Neuroinflammation. 12 (1): 46. doi:10.1186/s12974-015-0256-1. PMC 4359547. PMID 25889963.
  11. CYNTHIA MCKELVEY, Press Report, What’s the Role of Myelin Oligodendrocyte Glycoprotein in NMO?
  12. Sudarshini Ramanathanab Russell C.Dalea Fabienne Brilota, Anti-MOG antibody: The history, clinical phenotype, and pathogenicity of a serum biomarker for demyelination, Autoimmunity Reviews, Volume 15, Issue 4, April 2016, Pages 307-324, https://doi.org/10.1016/j.autrev.2015.12.004
  13. Ya, Yaping; et al. (2015). "Autoantibody to MOG suggests two distinct clinical subtypes of NMOSD". Science China Life Sciences. 59 (12): 1270–1281. doi:10.1007/s11427-015-4997-y. PMC 5101174. PMID 26920678.
  14. Martin S. Weber, Tobias Derfuss, Wolfgang Brück, Anti–Myelin Oligodendrocyte Glycoprotein Antibody–Associated Central Nervous System Demyelination—A Novel Disease Entity? August 2018, JAMA Neurol. 2018;75(8):909-910. doi:10.1001/jamaneurol.2018.1055
  15. Silvia Tenembaum et al. Spectrum of MOG Autoantibody-Associated Inflammatory Diseases in Pediatric Patients, Neurology April 6, 2015 vol. 84 no. 14 Supplement I4-3A
  16. Yaqing Shu Youming Long Shisi Wang Wanming Hu Jian Zhou Huiming Xu Chen Chen Yangmei Ou Zhengqi Lu Alexander Y. Lau Xinhua Yu Allan G. Kermode Wei Qiu, Brain histopathological study and prognosis in MOG antibody‐associated demyelinating pseudotumor, 08 January 2019, https://doi.org/10.1002/acn3.712
  17. Kakalacheva, Kristina; et al. (2016). "Infectious Mononucleosis Triggers Generation of IgG Auto-Antibodies against Native Myelin Oligodendrocyte Glycoprotein". Viruses. 8 (2): 51. doi:10.3390/v8020051. PMC 4776206. PMID 26907324.
  18. De Luca et al. Cross-reactivity between myelin oligodendrocyte glycoprotein and human endogenous retrovirus W protein: nanotechnological evidence for the potential trigger of multiple sclerosis, Micron Volume 120, May 2019, Pages 66-73, doi: https://doi.org/10.1016/j.micron.2019.02.005
  19. Spadaro Melania; et al. (2015). "Histopathology and clinical course of MOG-antibody-associated encephalomyelitis". Annals of Clinical and Translational Neurology. 2 (3): 295–301. doi:10.1002/acn3.164. PMC 4369279. PMID 25815356.
  20. Deena A. Tajfirouz, M. Tariq Bhatti, John J. Chen, Clinical Characteristics and Treatment of MOG-IgG–Associated Optic Neuritis Current Neurology and Neuroscience Reports, December 2019
  21. Nakashima, Ichiro (2015). "Anti-myelin oligodendrocyte glycoprotein antibody in demyelinating diseases". Clinical and Experimental Neuroimmunology. 6: 59–63. doi:10.1111/cen3.12262.
  22. S. Jarius et al. MOG encephalomyelitis: international recommendations on diagnosis and antibody testing, Journal of Neuroinflammation201815:134, https://doi.org/10.1186/s12974-018-1144-2
  23. Maciej Jurynczyk Ruth Geraldes Fay Probert Mark R. Woodhall Patrick Waters George Tackley Gabriele DeLuca Saleel Chandratre Maria I. Leite Angela Vincent, Distinct brain imaging characteristics of autoantibody-mediated CNS conditions and multiple sclerosis, Brain, Volume 140, Issue 3, 1 March 2017, Pages 617–627, https://doi.org/10.1093/brain/aww350, 24 February 2017
  24. Pérez CA, Garcia-Tarodo S, Troxell R. MRI-Negative Myelitis Associated With Myelin Oligodendrocyte Glycoprotein Antibody Spectrum Demyelinating Disease. Child Neurol Open. 2019;6:2329048X19830475. Published 2019 Feb 17. https://doi:10%5B%5D.1177/2329048X19830475
  25. Lekha Pandit et al., MOG-IgG-associated disease has a stereotypical clinical course, asymptomatic visual impairment and good treatment response, July 17, 2018, doi:10.1177/2055217318787829
  26. Oshiro A, Nakamura S, Tamashiro K, Fujihara K. Anti-MOG + neuromyelitis optica spectrum disorders treated with plasmapheresis, No To Hattatsu. 2016 May;48(3):199-203
  27. Rocio Vazquez do Campo, Ramon Yarza, Sebastian Lopez Chiriboga and Kevin Barrett, Myelin Oligodendrocyte Glycoprotein (MOG) Autoimmunity. A Case Report, Neurology April 5, 2016 vol. 86 no. 16 Supplement P5.346
  28. Miyazaki T, Nakajima H, Motomura M, Tanaka K, Maeda Y, Shiraishi H, Tsujino A., A case of recurrent optic neuritis associated with cerebral and spinal cord lesions and autoantibodies against myelin oligodendrocyte glycoprotein relapsed after fingolimod therapy. Rinsho Shinkeigaku. 2016 Apr 28;56(4):265-9. doi: 10.5692/clinicalneurol.cn-000756. Epub 2016 Mar 24. PMID 27010093
  29. Kezuka; et al. (2012). "Relationship Between NMO-Antibody and Anti–MOG Antibody in Optic Neuritis". Journal of Neuro-Ophthalmology. 32 (2): 107–110. doi:10.1097/WNO.0b013e31823c9b6c. PMID 22157536.
  30. Fujihara K, et al. (8 March 2018). "Myelin oligodendrocyte glycoprotein immunoglobulin G-associated disease: An overview". Clin. And Exp. Neuroinmunology. 9: 48–55. doi:10.1111/cen3.12434.
  31. Mader, S; Gredler, V; Schanda, K; et al. (2011). "Complement activating antibodies to myelin oligodendrocyte glycoprotein in neuromyelitis optica and related disorders". J Neuroinflammation. 8: 184. doi:10.1186/1742-2094-8-184. PMC 3278385. PMID 22204662.
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