case_images: PMC6768005_01
case_images: Baseline brain MRI in patients 1 and 2, performed during the first month of the disease. (A) Diffusion weighted sequences showing multiple deep and cortical acute microinfarcts in both patients (arrows). (B) FLAIR sequences showing no or minimal brain parenchymal lesions but high intensity signal in cortical sulci in patients 1 and 2 (arrows). (C) T2* sequences showing doubtful sulcal hypointensities in patient 1 and 5 microbleeds in patient 2 (arrows).
case_images: fneur-10-00984-g0001.jpg
case_images: PMC6768005_01_fneur-10-00984-g0001.jpg
case_images: F1
case_images: By contrast, multiple cortical and subcortical punctuate lesions on diffusion weighted imaging (DWI) sequences were present in both patients (Figure 1).
case_images: Meningeal biopsy in patient 1. Meningeal tissue section showing Abeta amyloid deposits in the wall of small meningeal arteries (brown staining) and a lymphocytic perivascular infiltrate (dark blue cells).
case_images: fneur-10-00984-g0002.jpg
case_images: PMC6768005_01_fneur-10-00984-g0002.jpg
case_images: F2
case_images: CAA-RI (Figure 2). Cortical vessels were sparred by inflammation.
case_images: Follow-up brain MRI in the 2 patients. T2* sequences at 1 year after the onset, in patient 1 and patient 2 showing increasing load of superficial microbleeds and hemosiderosis.
case_images: fneur-10-00984-g0003.jpg
case_images: PMC6768005_01_fneur-10-00984-g0003.jpg
case_images: F3
case_images: In contrast, on T2* sequences, a large number of microbleeds and several foci of cortical siderosis appeared in both cases as previously reported in cerebral amyloid angiopathy (Figure 3).