| Peer-Reviewed

A Case of Refractory Absence Epilepsy Precedes Anti-MOG Associated Optic Neuritis

Received: 5 April 2021     Accepted: 11 May 2021     Published: 27 May 2021
Views:       Downloads:
Abstract

Childhood absence epilepsy (CAE) is one of the most common forms of pediatric epilepsy. While most patients become seizure free with anti-epileptic drug therapy approximately 20% do not achieve seizure remission and are defined as having refractory CAE. Epilepsy is generally thought of as a grey matter disease but has also been associated with abnormal white matter. Optic neuritis (ON), on the other hand, is typically a white matter disorder characterized by inflammation and demyelination of the myelin sheath due to autoantibodies, such as the anti-myelin oligodendrocyte glycoprotein (MOG) antibody. We present the case of an 11-year-old female with refractory CAE who developed anti-MOG antibody positive ON. CAE and ON are not commonly co-morbid and to our knowledge their co-occurrence in a patient has not been previously described. However, in this case, the CAE and ON may be related as her seizures dramatically improved after initiating immunomodulatory treatments for the ON. This may indicate a relationship between ON (potentially specific to anti-MOG positive ON) and CAE, or may suggest that there is an inflammatory component to CAE and that immunomodulatory therapies may have a role in seizure control. Thus, in cases of treatment resistant absence epilepsy, an immune work up may be helpful.

Published in Clinical Neurology and Neuroscience (Volume 5, Issue 2)
DOI 10.11648/j.cnn.20210502.15
Page(s) 25-29
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2021. Published by Science Publishing Group

Keywords

Seizure, Childhood Absence Epilepsy, Neuroinflammation, Demyelination

References
[1] Posner E. Absence seizures in children. BMJ Clin Evid. Jan 10 2008; 2008.
[2] Arya R, Greiner HM, Lewis A, et al. Vagus nerve stimulation for medically refractory absence epilepsy. Seizure. May 2013; 22 (4): 267-70. doi: 10.1016/j.seizure.2013.01.008.
[3] Liang JS, Lee SP, Pulli B, et al. Microstructural Changes in Absence Seizure Children: A Diffusion Tensor Magnetic Resonance Imaging Study. Pediatr Neonatol. Aug 2016; 57 (4): 318-25. doi: 10.1016/j.pedneo.2015.10.003.
[4] Widjaja E, Kis A, Go C, Raybaud C, Snead OC, Smith ML. Abnormal white matter on diffusion tensor imaging in children with new-onset seizures. Epilepsy Res. Mar 2013; 104 (1-2): 105-11. doi: 10.1016/j.eplepsyres.2012.10.007.
[5] Foroozan R, Buono LM, Savino PJ, Sergott RC. Acute demyelinating optic neuritis. Curr Opin Ophthalmol. Dec 2002; 13 (6): 375-80.
[6] Dos Passos GR, Oliveira LM, da Costa BK, et al. MOG-IgG-Associated Optic Neuritis, Encephalitis, and Myelitis: Lessons Learned From Neuromyelitis Optica Spectrum Disorder. Front Neurol. 2018; 9: 217. doi: 10.3389/fneur.2018.00217.
[7] Chan CH, Briellmann RS, Pell GS, Scheffer IE, Abbott DF, Jackson GD. Thalamic atrophy in childhood absence epilepsy. Epilepsia. Feb 2006; 47 (2): 399-405. doi: 10.1111/j.1528-1167.2006.00435.x.
[8] Caplan R, Levitt J, Siddarth P, et al. Frontal and temporal volumes in Childhood Absence Epilepsy. Epilepsia. Nov 2009; 50 (11): 2466-72. doi: 10.1111/j.1528-1167.2009.02198.x.
[9] Rossi MA. Deep white matter track record of functional integrity in childhood absence epilepsy. Epilepsy Curr. Nov 2012; 12 (6): 234-5. doi: 10.5698/1535-7511-12.6.234.
[10] Hamid SHM, Whittam D, Saviour M, et al. Seizures and Encephalitis in Myelin Oligodendrocyte Glycoprotein IgG Disease vs Aquaporin 4 IgG Disease. JAMA Neurol. Jan 1 2018; 75 (1): 65-71. doi: 10.1001/jamaneurol.2017.3196.
[11] Zhong X, Zhou Y, Chang Y, et al. Seizure and Myelin Oligodendrocyte Glycoprotein Antibody-Associated Encephalomyelitis in a Retrospective Cohort of Chinese Patients. Front Neurol. 2019; 10: 415. doi: 10.3389/fneur.2019.00415.
[12] Gutman JM, Kupersmith M, Galetta S, Kister I. Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with optic neuritis and seizures. J Neurol Sci. Apr 15 2018; 387: 170-173. doi: 10.1016/j.jns.2018.01.042.
[13] Koh S. Role of Neuroinflammation in Evolution of Childhood Epilepsy. J Child Neurol. Jan 2018; 33 (1): 64-72. doi: 10.1177/0883073817739528.
[14] Choi J, Nordli DR, Jr., Alden TD, et al. Cellular injury and neuroinflammation in children with chronic intractable epilepsy. J Neuroinflammation. Dec 19 2009; 6: 38. doi: 10.1186/1742-2094-6-38.
[15] Dickstein LP, Liow JS, Austermuehle A, et al. Neuroinflammation in neocortical epilepsy measured by PET imaging of translocator protein. Epilepsia. Jun 2019; 60 (6): 1248-1254. doi: 10.1111/epi.15967.
[16] Sotgiu S, Murrighile MR, Constantin G. Treatment of refractory epilepsy with natalizumab in a patient with multiple sclerosis. Case report. BMC Neurol. Sep 23 2010; 10: 84. doi: 10.1186/1471-2377-10-84.
[17] Lapato AS, Szu J, Hasselmann JPC, Khalaj AJ, Binder DK, Tiwari-Woodruff SK. Chronic demyelination-induced seizures. Neuroscience. Jan 30 2017; 346: 409-422. doi: 10.1016/j.neuroscience.2017.01.035.
[18] Korff CM, Dale RC. The Immune System in Pediatric Seizures and Epilepsies. Pediatrics. Sep 2017; 140 (3) doi: 10.1542/peds.2016-3534.
[19] Kelley SA, Kossoff EH. Doose syndrome (myoclonic-astatic epilepsy): 40 years of progress. Dev Med Child Neurol. Nov 2010; 52 (11): 988-93. doi: 10.1111/j.1469-8749.2010.03744.x.
[20] Veggiotti P, Pera MC, Teutonico F, Brazzo D, Balottin U, Tassinari CA. Therapy of encephalopathy with status epilepticus during sleep (ESES/CSWS syndrome): an update. Epileptic Disord. Mar 2012; 14 (1): 1-11. doi: 10.1684/epd.2012.0482.
[21] Song JM, Hahn J, Kim SH, Chang MJ. Efficacy of Treatments for Infantile Spasms: A Systematic Review. Clin Neuropharmacol. Mar/Apr 2017; 40 (2): 63-84. doi: 10.1097/WNF.00000000000002.
Cite This Article
  • APA Style

    Katharina Blunschi, Pallavi Avasarala, John Schreiber, Neha Athale, Ilana Kahn, et al. (2021). A Case of Refractory Absence Epilepsy Precedes Anti-MOG Associated Optic Neuritis. Clinical Neurology and Neuroscience, 5(2), 25-29. https://doi.org/10.11648/j.cnn.20210502.15

    Copy | Download

    ACS Style

    Katharina Blunschi; Pallavi Avasarala; John Schreiber; Neha Athale; Ilana Kahn, et al. A Case of Refractory Absence Epilepsy Precedes Anti-MOG Associated Optic Neuritis. Clin. Neurol. Neurosci. 2021, 5(2), 25-29. doi: 10.11648/j.cnn.20210502.15

    Copy | Download

    AMA Style

    Katharina Blunschi, Pallavi Avasarala, John Schreiber, Neha Athale, Ilana Kahn, et al. A Case of Refractory Absence Epilepsy Precedes Anti-MOG Associated Optic Neuritis. Clin Neurol Neurosci. 2021;5(2):25-29. doi: 10.11648/j.cnn.20210502.15

    Copy | Download

  • @article{10.11648/j.cnn.20210502.15,
      author = {Katharina Blunschi and Pallavi Avasarala and John Schreiber and Neha Athale and Ilana Kahn and Tarannum Lateef},
      title = {A Case of Refractory Absence Epilepsy Precedes Anti-MOG Associated Optic Neuritis},
      journal = {Clinical Neurology and Neuroscience},
      volume = {5},
      number = {2},
      pages = {25-29},
      doi = {10.11648/j.cnn.20210502.15},
      url = {https://doi.org/10.11648/j.cnn.20210502.15},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cnn.20210502.15},
      abstract = {Childhood absence epilepsy (CAE) is one of the most common forms of pediatric epilepsy. While most patients become seizure free with anti-epileptic drug therapy approximately 20% do not achieve seizure remission and are defined as having refractory CAE. Epilepsy is generally thought of as a grey matter disease but has also been associated with abnormal white matter. Optic neuritis (ON), on the other hand, is typically a white matter disorder characterized by inflammation and demyelination of the myelin sheath due to autoantibodies, such as the anti-myelin oligodendrocyte glycoprotein (MOG) antibody. We present the case of an 11-year-old female with refractory CAE who developed anti-MOG antibody positive ON. CAE and ON are not commonly co-morbid and to our knowledge their co-occurrence in a patient has not been previously described. However, in this case, the CAE and ON may be related as her seizures dramatically improved after initiating immunomodulatory treatments for the ON. This may indicate a relationship between ON (potentially specific to anti-MOG positive ON) and CAE, or may suggest that there is an inflammatory component to CAE and that immunomodulatory therapies may have a role in seizure control. Thus, in cases of treatment resistant absence epilepsy, an immune work up may be helpful.},
     year = {2021}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - A Case of Refractory Absence Epilepsy Precedes Anti-MOG Associated Optic Neuritis
    AU  - Katharina Blunschi
    AU  - Pallavi Avasarala
    AU  - John Schreiber
    AU  - Neha Athale
    AU  - Ilana Kahn
    AU  - Tarannum Lateef
    Y1  - 2021/05/27
    PY  - 2021
    N1  - https://doi.org/10.11648/j.cnn.20210502.15
    DO  - 10.11648/j.cnn.20210502.15
    T2  - Clinical Neurology and Neuroscience
    JF  - Clinical Neurology and Neuroscience
    JO  - Clinical Neurology and Neuroscience
    SP  - 25
    EP  - 29
    PB  - Science Publishing Group
    SN  - 2578-8930
    UR  - https://doi.org/10.11648/j.cnn.20210502.15
    AB  - Childhood absence epilepsy (CAE) is one of the most common forms of pediatric epilepsy. While most patients become seizure free with anti-epileptic drug therapy approximately 20% do not achieve seizure remission and are defined as having refractory CAE. Epilepsy is generally thought of as a grey matter disease but has also been associated with abnormal white matter. Optic neuritis (ON), on the other hand, is typically a white matter disorder characterized by inflammation and demyelination of the myelin sheath due to autoantibodies, such as the anti-myelin oligodendrocyte glycoprotein (MOG) antibody. We present the case of an 11-year-old female with refractory CAE who developed anti-MOG antibody positive ON. CAE and ON are not commonly co-morbid and to our knowledge their co-occurrence in a patient has not been previously described. However, in this case, the CAE and ON may be related as her seizures dramatically improved after initiating immunomodulatory treatments for the ON. This may indicate a relationship between ON (potentially specific to anti-MOG positive ON) and CAE, or may suggest that there is an inflammatory component to CAE and that immunomodulatory therapies may have a role in seizure control. Thus, in cases of treatment resistant absence epilepsy, an immune work up may be helpful.
    VL  - 5
    IS  - 2
    ER  - 

    Copy | Download

Author Information
  • Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA

  • Trinity College of Arts and Sciences, Duke University, Durham, NC, USA

  • Department of Neurology, Children’s National Health System and George Washington University School of Medicine, Washington D. C., USA

  • Department of Neurology, Children’s National Health System and George Washington University School of Medicine, Washington D. C., USA

  • Department of Neurology, Children’s National Health System and George Washington University School of Medicine, Washington D. C., USA

  • Department of Neurology, Children’s National Health System and George Washington University School of Medicine, Washington D. C., USA

  • Sections