Signs & Symptoms
MOG antibody disease preferentially causes inflammation in the optic nerve,8 but can also cause inflammation in the spinal cord, brain, and brainstem.5 Symptoms can include:
- Loss or blurring of vision in one or both eyes
- Loss of color vision
- Paralysis (no motor function) of a limb or limbs
- Paraparesis (weakness) of a limb or limbs
- Loss of sensation
- Loss of bladder or bowel control
- Profound bladder retention
Those with MOG antibody disease are more likely to have both optic nerves affected at the same time, and if the symptoms are in only one eye, the other optic nerve may show subclinical atrophy.4
Children can be found to have the MOG antibody in the setting of ADEM; however, a positive MOG antibody test in the setting of ADEM does not necessarily imply a course of MOGAD. 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. When a relapse occurs, the diagnosis of MOGAD is confirmed.
MOG antibody disease can also occur in relation to another condition called anti-N-methyl-D-aspartate (NMDA) receptor encephalitis.1 NMDA receptor encephalitis is an autoimmune encephalitis that can cause psychosis, issues with memory and language, and seizures.1
One study described symptoms and MRI findings of MOG antibody disease in children under the age of 7 that were similar to leukodystrophies.10 Leukodystrophies are genetic rare diseases that affect the central nervous system by disrupting myelination.
(1) Fan S, Xu Y, Ren H, et al. Comparison of myelin oligodendrocyte glycoprotein (MOG)-antibody disease and AQP4-IgG-positive neuromyelitis optica spectrum disorder (NMOSD) when they co-exist with anti-NMDA (N-methyl-D-aspartate) receptor encephalitis. Mult Scler Relat Disord. 2018 Feb;20:144-152. doi: 10.1016/j.msard.2018.01.007. Epub 2018 Jan 31.
(4) Weber MS, Derfuss T, Metz I, Brück W. Defining distinct features of anti-MOG antibody associated central nervous system demyelination. Ther Adv Neurol Disord. 2018 Mar 29;11:1756286418762083. doi: 10.1177/1756286418762083. eCollection 2018.
(5) Lechner C, Baumann M, Hennes EM, et al. Antibodies to MOG and AQP4 in children with neuromyelitis optica and limited forms of the disease. J Neurol Neurosurg Psychiatry. 2016 Aug;87(8):897-905. doi: 10.1136/jnnp-2015-311743. Epub 2015 Dec 8.
(8) Cobo-Calvo A, Ruiz A, Maillart E, et al. Clinical spectrum and prognostic value of CNS MOG autoimmunity in adults: The MOGADOR study. Neurology. 2018 May 22;90(21):e1858-e1869. doi: 10.1212/WNL.0000000000005560. Epub 2018 Apr 25.
(9) Gutman JM, Kupersmith M, Galetta S, Kister I. Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with optic neuritis and seizures. J Neurol Sci. 2018 Apr 15;387:170-173. doi: 10.1016/j.jns.2018.01.042. Epub 2018 Feb 2.
(10) Hacohen Y, Rossor T, Mankad K, et al. ‘Leukodystrophy-like’ phenotype in children with myelin oligodendrocyte glycoprotein antibody-associated disease. Dev Med Child Neurol. 2018 Apr;60(4):417-423. doi: 10.1111/dmcn.13649. Epub 2017 Dec 30.