FIG 5.

ARIA-E interpretation pitfalls and mimics. A, Shading artifacts with prescan normalize inadvertently turned off, results in T2-FLAIR hyperintense signal in the bilateral occipital white matter (red arrows) that mimics ARIA-E (edema). B, Axial T2-FLAIR images from 2 time points with the 2 scans performed on different vendors. T2-FLAIR hyperintense signal in the bilateral occipital white matter on vendor 2 (red arrows) appears to be new from the prior examination on vendor 1 and may be mistaken for subtle ARIA-E. The participant returned for repeat imaging on vendor 1, and the apparent abnormality was resolved (not shown). C, Diffuse sulcal T2-FLAIR hyperintense signal with administration of supplemental oxygen mimics ARIA-E effusion. The abnormality resolved on repeat imaging without supplemental oxygen. D, Poor CSF suppression results in artifactual sulcal T2-FLAIR hyperintense signal mimicking ARIA-E (red arrow) and was confirmed to be artifacts by resolution on immediate repeat imaging with optimized parameters. E, Susceptibility artifacts from a hearing aid results in apparent T2-FLAIR hyperintense signal (red arrow), new from the prior examination on which the patient’s hearing aid was not in place. The third image in this set is the GRE scan showing the marked signal void artifacts from the hearing aid. The resulting susceptibility effect results in incomplete water suppression on T2-FLAIR, and the resulting artifacts mimic ARIA-E. F, Patient with left occipital subcortical T2-FLAIR hyperintense signal on the postdosing monitoring examination (mild ARIA-E, circle), which resolved on the follow-up monitoring scan. Separate subcentimeter focus of periventricular T2 signal with associated diffusion restriction (arrow, left) was consistent with an incidental acute/subacute infarct that showed expected evolution on the postdosing follow-up examination (right). Images courtesy of Biogen and the Dominantly Inherited Alzheimer Network. Supp indicates supplemental.