PMC8334553_01
The timeline with relevant data of the past episodes and interventions. *Severe relapse treated with plasma exchange. #This admission. AZA, azathioprine; TAC, tacrolimus.
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The detailed timeline with relevant data of the past episodes and interventions was summarized in  Figure 1 .
MRI of the NMOSD lesions. MRI of the cervical and thoracic spine showed a longitudinally extensive T2-hyperintense lesion [(A, B), white arrows], which involved the central portion of the cord [(C), white arrowhead]. A significant enhancement and thickening of the bilateral optic nerve sheaths were observed [(D), yellow arrows].
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MRI of the cervical and thoracic spine showed a longitudinally extensive T2-hyperintense lesion, with the central portion of the cord involved ( Figures 2A-C ). A significant enhancement and thickening of the optic nerve sheaths were also observed ( Figure 2D ).
The changes in serum AQP4-IgG levels performed by cell-based assay before and after each protein-A immunoadsorption treatment (A) and the changes in serum concentration of immunoglobulins and complement proteins before and after each session (B). Each treatment could lead to a significant decline in the serum AQP4-IgG titer, IgA, IgG, IgM, as well as C3 and C4 levels, with a slight rebound before the next therapy.
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AQP4-IgG tested by cell-based assay (CBA) revealed a positive result, with a titer of 1:320 in the serum ( Figure 3A ) and 1:1 in the CSF, while the myelin oligodendrocyte glycoprotein antibody (MOG-IgG), glial fibrillary acidic protein antibody (GFAP-IgG), myelin basic protein antibody (MBP-IgG), AQP1-IgG, and Flottilin1/2-IgG in the serum and CSF, which were also measured by CBA, were undetectable. The results revealed that each treatment could lead to a significant reduction in the AQP4-IgG titer, while a slight rebound was always observed before the start of the next therapy ( Figure 3A ). The IgG, IgA, IgM, C3, and C4 demonstrated almost the same trends ( Figure 3B ).