Article Figures & Data
Figures
- Fig 1.
Imaging of CAA/ACNS at presentation and after 9 months of therapy with pathologic correlation.
A, FLAIR coronal image shows increased signal intensity with mass effect on the adjacent sulci and lateral ventricles in the right occipitotemporal region.
B, Diffusion-weighted axial image shows no restricted diffusion.
C, T1-weighted axial contrast-enhanced image shows decreased signal intensity without contrast enhancement.
D, Probe-press, single voxel (2 cm3 [TE = 135]) centered on the region of abnormality shows normal spectra and ratios.
E, Hematoxylin and eosin slide shows a blood vessel (arrow) with surrounding inflammation and multinucleated giant cells (arrowheads).
F, Immunohistochemistry with a beta-amyloid specific antibody demarcates the vessel wall (arrowheads). Both vessels are surrounded by a mononuclear inflammatory infiltrate (hematoxylin counter-stain).
G, FLAIR coronal image obtained 9 months after presentation shows significant resolution of previously seen tumafactive lesion in the right occipitotemporal region.
H, FLAIR axial image obtained 9 months after presentation shows increased signal intensity in the right and left temporal regions (arrows).
- Fig 2.
Multi-modality imaging of CAA at presentation and after treatment with pathologic correlation.
A, Noncontrast CT scan from 1999 shows decreased attenuation with sulcal effacement and mass effect on the occipital horn of the lateral ventricle.
B, T2-weighted axial image also from 1999 shows increased signal intensity with mass effect on the adjacent sulci and the right lateral ventricle.
C, Diffusion-weighted axial image shows no restricted diffusion.
D, T1-weighted axial contrast-enhanced image shows decreased signal intensity without enhancement.
E, Probe-press single voxel (2 cm3 [TE = 135]) centered on the region of abnormality shows normal spectra and ratios.
F, T2-weighted axial image obtained in 2000 shows near-complete resolution of right occipital abnormality with a small residual area of encephalomalacia at the biopsy site.
Tables
Previous case reports with MR imaging of CAA and CAA/ACNS
Series Pathology Contrast Enhancement Location Age Sex Antecedent Event Vandermissen et al (3) CAA No Supratentorial, abuts ependyma 46 recurred @ 59 M ICH Osumi et al (4) CAA No Supratentorial, abuts ependyma 56 recurred @ 59 F Seizure Ortiz and Reed (5) CAA No Supratentorial, abuts ependyma 68 F Safriel CAA No Supratentorial, abuts ependyma 71 F ‘Stroke’ Safriel CAA/ACNS No Supratentorial, abuts ependyma 48 M Tamargo et al (6) CAA/ACNS Slight Multiple supratentorial, abuts ependyma 80 F Polivka et al (7) CAA/ACNS No Supratentorial, abuts dura 60 M Polivka et al (7) CAA/ACNS No Supratentorial, abuts dura 74 F Fountain and Eberhard (8) CAA/ACNS No Multiple supratentorial, abuts ependyma 66 M ICH Note.—Caa, cerebral amyloid angiopathy; ACNS, angitis of the central nervous system; ICH, intracranial hemorrhage.
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