2021
DOI: 10.3345/cep.2020.01963
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Myelin oligodendrocyte glycoprotein antibody encephalitis following severe acute respiratory syndrome coronavirus 2 in a pediatric patient

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Cited by 18 publications
(31 citation statements)
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References 10 publications
(14 reference statements)
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“…One of the most plausible proposed mechanisms was a molecular mimicry in response to the SARS-CoV-2 infection which led to activation of host antibodies that cross-reacted and identified self antigens as foreign and cause damages to various system, including the central nervous system (CNS) [ 13 ]. There were various anti-neuronal autoantibodies that have been discovered to affect the nervous system in SARS-CoV-2 infected patients, namely the anti-N-methyl-D-aspartate-receptor (NMDAR) antibody [ 14 – 19 ], anti-contactin-associated protein-like-2 (CASPR2) antibodies [ 20 ], anti-myelin oligodendrocyte glycoprotein (MOG) antibody [ 21 , 22 ], anti-glutamic acid decarboxylase (GAD) antibody [ 23 ], anti-GD1a antibody [ 24 ] and many others. This mechanism was also suggested to explain other neurological complications of SARS-CoV-2 infection, namely Guillain–Barré syndrome [ 25 ] and acute disseminated encephalomyelitis [ 26 ], which further support the theory of molecular mimicry as the pathophysiology of autoimmune encephalitis.…”
Section: Resultsmentioning
confidence: 99%
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“…One of the most plausible proposed mechanisms was a molecular mimicry in response to the SARS-CoV-2 infection which led to activation of host antibodies that cross-reacted and identified self antigens as foreign and cause damages to various system, including the central nervous system (CNS) [ 13 ]. There were various anti-neuronal autoantibodies that have been discovered to affect the nervous system in SARS-CoV-2 infected patients, namely the anti-N-methyl-D-aspartate-receptor (NMDAR) antibody [ 14 – 19 ], anti-contactin-associated protein-like-2 (CASPR2) antibodies [ 20 ], anti-myelin oligodendrocyte glycoprotein (MOG) antibody [ 21 , 22 ], anti-glutamic acid decarboxylase (GAD) antibody [ 23 ], anti-GD1a antibody [ 24 ] and many others. This mechanism was also suggested to explain other neurological complications of SARS-CoV-2 infection, namely Guillain–Barré syndrome [ 25 ] and acute disseminated encephalomyelitis [ 26 ], which further support the theory of molecular mimicry as the pathophysiology of autoimmune encephalitis.…”
Section: Resultsmentioning
confidence: 99%
“…Six (20%) of the patients were from paediatric age, defined as 12 years and younger [ 18 , 21 – 23 , 26 ]. Amongst the most commonly reported neurological presentation of autoimmune encephalitis in SARS-CoV-2 infection are altered mental status [ 21 , 30 , 32 , 36 – 39 , 41 – 44 , 47 ], psychomotor agitation [ 14 , 15 , 20 ], memory deficit [ 20 , 30 , 36 ], some form of psychogenic disturbance like hallucinations or delusions [ 14 16 , 23 , 46 ], ataxia [ 19 , 24 , 26 , 31 , 33 ] and seizure [ 15 18 , 20 22 , 36 , 37 , 42 , 43 , 45 , 47 ]. Based on the typical findings on magnetic resonance imaging scan of the brain, six of the patients had limbic encephalitis [ 36 – 38 , 42 , 43 ], three had cerebellitis [ 24 , 31 , 39 ] and one had brain stem encephalitis [ 33 ].…”
Section: Resultsmentioning
confidence: 99%
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“…Clinical presentations include fever, headache, conscious disturbance, seizure, and behavioral change. Numerous cases of COVID-19 associated encephalitis have been reported [ 9 , [11] , [12] , [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] , [21] , [22] , [23] , [24] ]. Electron microscopic evidence of SARS-CoV-2 inclusions has been found in the cerebellum in a child with acute COVID-19 infection [ 9 ].…”
Section: Mr Neuroimagingmentioning
confidence: 99%
“…[ 10 ]. Numerous case reports have indicated the presence of acute encephalopathy or encephalitis [ [11] , [12] , [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] , [21] , [22] , [23] , [24] ], acute necrotizing encephalopathy (ANE) [ 25 , 26 ], acute disseminated encephalomyelitis (ADEM) [ 20 , [26] , [27] , [28] , [29] , [30] , [31] , [32] ], cytotoxic lesions in the callosal splenium [ 26 , [33] , [34] , [35] , [36] , [37] ], posterior reversible encephalopathy syndrome (PRES) [ 26 , 38 ], cerebral venous thrombosis [ 39 , 40 ], vasculitis and acute infarction [ 20 , 21 , [41] , [42] , [43] , [44] , [45] , [46] , [47] ], Guillain–Barré syndrome (GBS) [ 20 , 21 , 26 , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] ] and its variant Miller-Fisher syndrome (MFS) [ [59] , [60] , [61] , [62] ], transverse myelitis [ 9 , 50 ,…”
Section: Introductionmentioning
confidence: 99%