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. 2022 Sep;43(9):E19–E35. doi: 10.3174/ajnr.A7586

FIG 4.

FIG 4.

Atypical ARIA-E, parenchymal edema. Axial T2-FLAIR images from 3 separate patients at pretreatment baseline (left) and on a monitoring examination following initiation of anti-amyloid monoclonal antibody therapy (postdosing, right). A, Adjacent slices on postdosing T2-FLAIR show development of multiple nodular areas of ARIA-E (red arrows). This nodular presentation is less commonly encountered in contrast to the typical ARIA-E, which has an amorphous parenchymal pattern as expected for vasogenic edema. In this case, although each area of ARIA-E is small (<5 cm), the multiplicity of lesions yields a classification of moderate ARIA-E. B, Atypical ARIA-E as a rounded focus of T2-FLAIR hyperintense signal in the left parietal white matter (left, red arrow) that may be mistaken for neoplastic process and differentiated by the time course of appearance coinciding with monoclonal antibody dosing and subsequent resolution. C, Atypical ARIA-E in the cerebellar vermis. Postdosing, new T2-FLAIR hyperintense signal in the cerebellar vermis (red arrow), a less common location for ARIA-E relative to the cerebral hemispheres. Although ARIA-E has a slight predilection for the parieto-occipital lobes, similar to posterior reversible encephalopathy, any part of the brain may be affected. Images courtesy of Biogen and the Dominantly Inherited Alzheimer Network.