Does area postrema syndrome occur in myelin oligodendrocyte glycoprotein-IgG-associated disorders (MOGAD)?

摘要

Myelin oligodendrocyte glycoprotein-IgG is a biomarker associated with CNS demyelinating diseases.1,2 MOGAD and aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4-IgG + NMOSD) have overlapping clinical features including optic neuritis and myelitis. However, there are several clinical and radiologic distinguishing features of MOGAD including lack of female predominance, higher incidence of acute disseminated encephalomyelitis (ADEM), higher proportion of bilateral optic neuritis, and T2-signal confined to gray matter and conus involvement in myelitis. The 2015 International Panel criteria for NMOSD delineate 6 core clinical characteristics including area postrema syndrome (APS). 5APS is characterized by intractable nausea, vomiting, and hiccups (INVH) for >48 hours and can occur in isolation with discrete T2/FLAIR and T1 gadolinium-enhancing lesions involving the area postrema.6 It has been reported to occur clinically in isolation at onset in 7.1%-10.3% and throughout the disease in 9.4%-14.5%.