A 21-year-old man presented with fever and headache in April 2013. Cerebrospinal fluid (CSF) showed pleocytosis, and magnetic resonance imaging revealed T2 hyperintensity in the bilateral cerebellar peduncles (Picture A, B). The patient's condition gradually improved without medication. In August, November, and December 2017, he experienced dizziness and unsteadiness of gait with a left cerebellar lesion (Picture C, D), bilateral cerebellar lesions (Picture E, F), and a right cerebellar peduncle lesion (Picture G, H), respectively, and the CSF showed pleocytosis. He responded well to methylprednisolone pulse therapy, and we initiated oral prednisolone after determining negativity for anti-SS-A, anti-SS-B, anti-thyroid peroxidase, anti-thyroglobulin, anti-glutamic acid decarboxylase, and anti-aquaporin-4 antibodies, and positivity for antibodies against myelin oligodendrocyte glycoprotein (MOG). In April 2019, he experienced bilateral cerebellar peduncle relapse because of drug noncompliance (Picture I, J). Although MOG antibody-associated disease (MOGAD) with cerebellitis has been reported (1,2), this patient notably had recurrent cerebellar lesions for over seven years. Furthermore, no relapse occurred after starting oral steroids, highlighting the importance of evaluated the anti-MOG antibody status in cases of recurrent cerebellitis. Cerebellar peduncles are reportedly an early site of myelination during brain development (3,4). We therefore speculate that the MOG expression is high in cerebellar peduncle and hemisphere.
Picture.
The authors state that they have no Conflict of Interest (COI).
Teruyuki Ishikura and Tatsusada Okuno contributed equally to this work.
Acknowledgement
We thank Kimihiko Kaneko for the measurement of anti-MOG antibody and Taro Higuchi for the English language editing.
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