Abstract

Cerebral amyloid angiopathy (CAA) is a common type of cerebral small vessel disease and a key cause of spontaneous lobar intracerebral hemorrhage (ICH) in the elderly.1,2 Currently, the clinical diagnosis of probable CAA is based on characteristic imaging findings including strictly lobar ICH and CAA-associated hemorrhagic lesions (e.g., cerebral microbleeds [CMB] and cortical superficial siderosis). Despite their high specificity for CAA,3 these lesions only provide indirect evidence of advanced disease. Currently, a definite CAA diagnosis can only be obtained on a brain biopsy or with a neuropathologic examination of the brain postmortem. Quantifying potential early stages of CAA in vivo through more direct biomarkers remains challenging.4 In order to assess the diagnostic yield of a direct amyloid PET tracer in the clinical setting, in the Journal club article “Florbetapir imaging in cerebral amyloid angiopathy-related hemorrhages,” Raposo and colleagues compared cortical florbetapir-PET retention between patients with CAA-related ICH and patients with hypertension-related deep ICH. The authors report increased cortical florbetapir-PET uptake in patients with CAA-related ICH compared to those with deep ICH. However, its diagnostic value in acute CAA-related ICH was proved to be limited by its moderate sensitivity and specificity. While these data do not yet have direct implications for CAA in clinical practice, they are useful in consolidating evidence on amyloid-PET performance in the setting of symptomatic CAA-related lobar ICH and may be informative for guiding future studies and trials in CAA.4

Full Text
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