Table 1.

Clinical features of patients with coexistence of antibodies of MOG and anti-NMDAR.

	Pérez, CA. 2020[9]	Zhou, L. 2017[10]	Aoe, S. 2019[12]	Zhou, J. 2018[13]	Sarigecili, E. 2019[14]
Age/sex	29-year-old/male	31-year-old/male	36-year-old/female	54-year-old/male	6-year old/male
Primary symptoms	Headache, fever, seizure, blurry vision, urinary retention, gait instability, and slurred speech in the 1st episode; bilateral painless blurry vision in the 2nd episode	Headache, seizure, fever, and headache in the 1st and the 2nd onset, respectively; right side anesthesia and continuous hiccup in the 3rd onset; blurred vision in the 4th onset	Headache, epilepsy, ataxia, depression, delusions, fever,somnolence, dyskinesia in the 1st onset; hallucinations, restlessness, tachycardia, hyperhidrosis, central apnea in the 2nd onset	Progressive dizziness, unsteadiness, narcoleptic attacks; light-headedness and intermittent spinning sensations	Alteration of gait, speech, behavior (agitation, aggression, irritability), and insomnia
Location of lesions in MRI	Lesions in mesial temporal lobe in the 1st onset; lesions in the left thalamus, optic chiasm, optic nerve, and the optic tracts in the 2nd onset	Lesions in the right temporal, parietal, and occipital cortex	Lesions in the medial aspect of the bilateral frontal lobes in the 1st onset; lesions in the basal ganglia, temporal lobe, cerebellum in the 2nd onset	Multiple lesions involvingthe bilateral cerebellum, right cerebral peduncle, and the brain parenchyma surrounding the third ventricle	Brain and spinal MRI findings were normal
Results of CSF	A mildly elevated level of protein, an elevated white blood cell count	Elevated leucocytes (80% mononuclear) and elevated protein	Protein level is unknown, mildly elevated leucocytes in the 1st and the 2nd onset	Normal opening pressure, with mild leukocytosis and elevated protein levels	No cells, normal protein and glucose levels
Cancer	No	No mention	No	Unremarkable	No mention
EEG	Unremarkable	Epileptic discharges exist	No mention	No abnormalities	Intermittent spike waves
Antibody detection	CSF anti-NMDAR-Ab (1:16); serum MOG-Ab (1:1000)	Serum anti-MOG (1:320); CSF NMDAR-Ab (1:1); OB (–)	CSF NMDAR-Ab (+) in the 1st and the 2nd episode (1:20); serum MOG-Ab (+) in the two episodes; OB (+)	CSF NMDAR-Ab (1:32); serum MOG-IgG (1:320);IgG index was 0.62; OB (–).	CSF anti-NMDAR-Ab and serum anti-MOG-Ab (1:320) all (+); OB (+); an elevated IgG index
Immunotherapy	Oral corticosteroids were initially used, and then1 course of IVMP (1 g/d × 5 days) in the 1st onset; a 5-day course of PE in the 2nd episode	IV DSM (10 mg/d) in the 1st onset; MP (80 mg/d × 2 weeks) in the 2nd onset.	3 courses of IVMP (1 course: 1 g/d × 3 days) and 1 course (0.4 g/kg × 5 days) of IVIg in the 1st onset; 2 courses of MP and PE, 1 course of IVIg in the 2nd onset.	IVMP (0.5 g/d × 3 days), and IVIG (0.4 g/kg/d × 5 days), followed by IV rituximab (0.6 g/week × 3 weeks).	MP (30 mg/kg × 3 days), followed by (20 mg/kg × 2 days).
Treatmentoutcomes	The symptoms improved after IVMP in the 1st onset. Neurological exam was normal at follow-up in the 2nd onset	The symptoms relieved after IV DSM in the 1st onset. His symptoms relieved in the 2nd episode	On the 81st day, she was discharged without sequelae in the 1st onset; relief of most symptoms in the 2nd onset	A mild gait disturbance at discharge. Resolution of most lesions at 2 months after discharge and symptomatic relief	Consciousness resumed on the 3rd day of the treatment. The patient was discharged with full recovery
Actual diagnosis and the reasons	Overlapping MOG-AD and anti-NMDARe existed in the 1st onset, MOG-AD existed in the 2nd onset.Reasons: Simultaneously meeting the diagnostic criteria of anti-NMDARe and MOG-AD, and involvement of opticnerves in the 1st onset	Anti-NMDARe existed in the 1st to the 3rd onset; MOG-AD existed in the 4th onset.Reasons: Coexistence of encephalopathy and no MOG-Ab in the 1st to the 3rd onset; optic neuritis; and good response to immunotherapy existed in the 4th onset	Anti-NMDARe existed in the 1st episode, and anti-NMDARe reappeared 3.5 years later.Reasons: She met the diagnostic criterion[6] of anti-NMDARe;she did not have a good response toimmunotherapy; vision was unaffected	The more likely diagnosis was anti-NMDARe.Reasons: Encephalopathy existed; the patient had a poor response to multiple rounds of immunotherapy; vision is unaffected	The more likely diagnosiswas MOG-AD involving the hemicerebrum.Reasons: Good responseto immunotherapy. It did not meet the diagnostic criterion[6] of typical anti-NMDARe