Additional studies have pointed out that NMDAR and MOG autoantigens may be simultaneously present on the surface of oligodendrocytes, which means that these two types of antibodies can coexist in one patient ( 12, 13). Therefore, both anti-NMDAR and anti-MOG antibodies are responsible for encephalitis. However, the highly sensitive and specific method for MOG antibody detection using cell-based assays (CBA), along with the new diagnostic criteria for similar neuroinflammatory diseases, has made it possible to identify MOG-AD as an independent entity distinct from other demyelinating diseases ( 10, 11). MOG antibody is initially delineated in demyelinating diseases such as multiple sclerosis, neuromyelitis optica, and acute disseminated encephalomyelitis, and is regarded as an assistant antibody that may worsen outcomes ( 6, 9). Moreover, anti-NMDAR antibodies could also be found in MOG antibody disease (MOG-AD) ( 8).
Myelin oligodendrocyte glycoprotein (MOG) antibody is an important concomitant antibody that may target oligodendrocytes in NMDAREs ( 6, 7). With the deeper recognition of NMDARE, some researchers have found that concomitant antibodies play a role in the progression of the disease ( 5). Although the incidence of the disease is estimated to be 1.5 per million population per year, this entity has garnered great attention in recent years owing to its specific clinical features and laboratory test results that cannot be explained by other, traditional encephalitis disorders ( 4). Anti-NMDAR encephalitis (NMDARE) commonly causes a variety of neuropsychiatric symptoms, including psychiatric symptoms, behavioral abnormalities, seizures, speech disorders, and decreased consciousness ( 2, 3). The overall symptoms seemed to be similar to those of NMDAR encephalitis.Īnti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is an immune-mediated disease characterized by the presence of specific cerebrospinal fluid (CSF) IgG antibodies against GluN1 subunits ( 1). In conclusion, anti-NMDAR-IgG +/MOG-IgG + was rarely observed, but the incidence rate of relapse was very high. 31.3% of patients presented with unilateral cerebral cortical encephalitis with epilepsy and 12.5% displayed bilateral frontal cerebral cortex encephalitis. The common MRI changes were in the cortex or subcortex (70.7%) and brainstem (31.0%). Relapse occurred in 63.4% of anti-NMDAR-IgG +/MOG-IgG + patients, in whom 50.0% of cases relapsed with encephalitic manifestations, and 53.8% relapsed with demyelinating manifestations. The prominent clinical symptoms were encephalitic manifestations, including seizures (56.9%) and abnormal behavior (51.7%), rather than demyelinating manifestations, such as speech disorder (34.5%) and optic neuritis (27.6%). The median of CSF anti-NMDAR antibody titer was 32, and the serum anti-MOG antibody titer was 100. The incidences (95%CI) of anti-NMDAR-IgG +/MOG-IgG + in the patients with serum MOG-IgG + and CSF anti-NMDAR-IgG + were 0.09 (0.02–0.19) and 0.07 (0.01–0.19), respectively. Nine observational studies and 16 case reports (58 cases with anti-NMDAR-IgG +/MOG-IgG +, 21.0 years, male 58.6%) were included.
#Anti mog prognosis software#
Stata software (version 15.0 SE) was used for the analyses. A pooled analysis was conducted with the fixed-effects model using the Mante-Haenszel method ( I 2 ≤ 50%), or the random-effects model computed by the DerSimonian–Laird method ( I 2 > 50%). We searched several databases for related publications published prior to April 2021.
This study aimed to perform a secondary analysis to determine the clinical features of this disease. 2Department of Neurology, Tianjin Huanhu Hospital, Tianjin, ChinaĬoexisting anti-NMDAR and MOG antibody (anti-NMDAR-IgG +/MOG-IgG +)-associated encephalitis have garnered great attention.1Department of Neurology, Tianjin Medical University General Hospital, Tianjin, China.
Jiayue Ding 1 * Xiangyu Li 2 Zhiyan Tian 2
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