Advances in cerebral amyloid angiopathy imaging

Szu-Ju Chen, Hsin-Hsi Tsai, Li-Kai Tsai, Sung-Chun Tang, Bo-Chin Lee, Hon-Man Liu, Ruoh-Fang Yen, Jiann-Shing Jeng, Szu-Ju Chen, Hsin-Hsi Tsai, Li-Kai Tsai, Sung-Chun Tang, Bo-Chin Lee, Hon-Man Liu, Ruoh-Fang Yen, Jiann-Shing Jeng

Abstract

Cerebral amyloid angiopathy (CAA) is a cerebral small vessel disease caused by β -amyloid (Aβ) deposition at the leptomeningeal vessel walls. It is a common cause of spontaneous intracerebral hemorrhage and a frequent comorbidity in Alzheimer's disease. The high recurrent hemorrhage rate in CAA makes it very important to recognize this disease to avoid potential harmful medication. Imaging studies play an important role in diagnosis and research of CAA. Conventional computed tomography and magnetic resonance imaging (MRI) methods reveal anatomical alterations, and remains as the most reliable tool in identifying CAA according to modified Boston criteria. The vascular injuries of CAA result in both hemorrhagic and ischemic manifestations and related structural changes on MRI, including cerebral microbleeds, cortical superficial siderosis, white matter hyperintensity, MRI-visible perivascular spaces, and cortical microinfarcts. As imaging techniques advance, not only does the resolution of conventional imaging improve, but novel skills in functional and molecular imaging studies also enable in vivo analysis of vessel physiological changes and underlying pathology. These modern tools help in early detection of CAA and may potentially serve as sensitive outcome markers in future clinical trials. In this article, we reviewed past studies of CAA focusing on utilization of various conventional and novel imaging techniques in both research and clinical aspects.

Keywords: cerebral amyloid angiopathy; cerebral microbleed; magnetic resonance imaging; positron emitting tomography; small vessel disease.

Conflict of interest statement

Conflict of interest statement: The authors declare that there is no conflict of interest.

Figures

Figure 1.
Figure 1.
Hemorrhagic presentations in cerebral amyloid angiopathy. (a) Brain computed tomography shows a left frontal lobar intracerebral hemorrhage with irregular hematoma border and finger-like projection. (b) SWI shows numerous lobar cerebral microbleeds restricted at corticosubcortical areas. (c) T2-FLAIR MRI shows a hyperintense lesion within sulci of cortical surface (arrow), indicating convexity subarachnoid hemorrhage. (d) Cortical superficial siderosis is revealed by SWI as hypointense curvilinear signals along the cortical gyri (arrows). FLAIR, fluid-attenuated inversion recovery; MRI, magnetic resonance imaging; SWI, susceptibility-weighted imaging.
Figure 2.
Figure 2.
Ischemic presentations in cerebral amyloid angiopathy. (a) T2-FLAIR MRI shows white matter hyperintensities with posterior predominant pattern (arrows). (b) MRI-visible perivascular spaces located at centrum semiovale are depicted on T2-weighted MRI as hyperintense signals with linear or dot-like appearance. (c) T2-FLAIR MRI shows ovoid lesions with hyperintense rim at periventricular areas, suggestive of lacunar infarcts. (d) High resolution diffusion-weighted imaging study shows a hyperintense dot in the cortical region, indicative of cortical microinfarct. (e) Progressive brain volume loss is shown on longitudinal follow up of T1-MRI studies in 2 years. FLAIR, fluid-attenuated inversion recovery; MRI, magnetic resonance imaging.
Figure 3.
Figure 3.
Amyloid-PET in cerebral amyloid angiopathy. PiB PET in patients with CAA, AD and hypertensive angiopathy. In contrast with patients with hypertensive angiopathy who do not have increased PiB uptake, patients with CAA and AD have higher global PiB retention. Compared with patients with AD, PiB distribution in CAA has a posterior predominant pattern. AD, Alzheimer’s disease; CAA, cerebral amyloid angiopathy; PET, positron emission tomography; PiB, C-Pittsburgh compound B.

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