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. 2021 Sep 14;97(11):e1097–e1109. doi: 10.1212/WNL.0000000000012467

Figure 2. Brain MRI T2 Lesion Evolution in Aquaporin 4–Immunoglobulin G–Positive Neuromyelitis Optica Spectrum Disorder (AQP4-IgG-NMOSD), Myelin Oligodendrocyte Glycoprotein–Immunoglobulin G–Associated Disorder (MOGAD), and Multiple Sclerosis (MS).

Figure 2

Axial fluid-attenuated inversion recovery infratentorial (A, C, E) and supratentorial (B, D, F) brain MRI are shown. In patients with AQP4-IgG-NMOSD (A, B), large acute lesions (A.a, B.a) commonly show a prominent reduction of their initial size but rarely resolve completely, typically leaving tiny residual abnormalities (A.b, B.b; red circles). In patients with MOGAD (C, D), most large acute T2-hyperintense lesions (C.a, D.a) resolve to undetectable (C.b) at follow-up MRI, although some acute T2 lesions can leave some (often nonspecific) small foci of T2 hyperintensity (D.b; red circle). In patients with MS (E, F), acute T2-hyperintense lesions are relatively smaller (E.a, F.a) and typically show moderate reduction in size at follow-up, while remaining clearly detectable (E.b, F.b; red circles).