MRI was performed using a1.5 T scanner according to routine clinical protocols and acquisition parameters as described.12 Sequences included axialFLAIR-weighted, fast-spin echo T2-weighted, gradient-echosusceptibility-weighted, and pregadolinium T1-weighted images. Postgadolinium T1-weighted images were obtained in 8 of12 subjects with available neuroimaging, and diffusionweighted images including maps of apparent diffusion coefficient (ADC) were obtained in 9.T2-weighted hyperintense lesions were segmented preferentially on FLAIR sequences and the lesion volume computed andnormalized to head size by two readers blinded to clinical characteristics as described.12,13 For comparison of the qualitativeMRI features of CAA-related inflammation vs noninflammatory CAA or RPL, groups of MRI scans were presented to anexperienced, CAQ-certified neuroradiologist without knowledge of the clinical diagnosis. Each group of scans was systematically characterized for lesion location, extent, T1 and T2intensity, and symmetry.