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•Anti-NMDAR encephalitis coexisted with anti-MOG antibody (MOG-Ab)-associated disease.•This case showed symptoms due to MOG-Ab followed by anti-NMDAR encephalitis.•The symptoms due to MOG-Ab were balance disability and word-finding difficulty.•MOG-Ab testing should be performed in anti-NMDAR encephalitis with atypical symptoms.

Summary Cortical somatosensory evoked potentials (c-SEP) and flash visual evoked potentials (f-VEP) were serially recorded in acute monophasic and chronic relapsing experimental allergic encephalomyelitis (EAE) in the Lewis rat. In acute EAE, a significantly delayed latency and broadened peak of the c-SEP were observed corresponding to the clinical onset, and then returned to normal with the disappearance of clinical signs. In chronic EAE, the c-SEP showed the same changes as in acute EAE, also reflecting the first attack, remission and relapsing phase. However, chronic EAE, when paralysis had recovered in the relapsing phase, showed c-SEP abnormalities suggestive of subclinical active lesions. In contrast, the f-VEP showed no obvious abnormalities in acute or chronic EAE. These findings suggest that the c-SEP is an objective and sensitive index for detecting clinical and pathological changes in acute and chronic EAE in the Lewis rat.

•Ant-MOG antibody (MOG-Ab) is produced mostly extrathecally.•MOG-Ab-associated diseases have been confirmed by its Ab serum assay.•Some patients demonstrate MOG Ab positivity only in CSF, but not in serum.•Additional Ab measurement in CSF might prevent the underdiagnosis of MOG-Ab diseases.

This report describes an 11-year-old girl with recurrent syncope beginning at the age of 2 1/2 years. Her paternal grandmother, father, and three of her five natural siblings had similar symptoms, often linked to emotional upsets. There were three adopted children from a single family, and none of these had syncope. Prior to referral there was an increase in attacks, some with convulsions, but with no other features of epilepsy. Vasovagal syncope was confirmed. However, continuous electroencephalogram, blood pressure, and heart rate recordings during attacks indicated that in some episodes there was neither cardiovascular change nor epileptiform activity, implying feigned syncope (pseudosyncope) with pseudoseizures. A psychological origin was sought, found, and in part rectified. The separation of vasovagal syncope from pseudosyncope, in the context of the family history, is discussed.