Imaging description

Cerebral amyloid angiopathy (CAA) is a heterogeneous group of biochemically and genetically diverse disorders that is characterized by the deposition of β-amyloid protein in the media and adventitia of small and medium-sized vessels of the cerebral cortex, subcortex, and leptomeninges. The deposition of amyloid results in weakening of blood vessels, leading to both asymptomatic microbleeds and symptomatic lobar intracerebral hemorrhage (ICH). CAA is a common cause of lobar hemorrhage in normotensive elderly patients [1].

On non-contrast CT, hematomas are easily identified and are typically noted in the cortex or subcortical region. Deep white matter, basal ganglia, and brainstem are generally spared. Other neuroimaging features that support a diagnosis of CAA include multiplicity and recurrent nature of lobar hematomas. The hematomas may be accompanied by subarachnoid, intraventricular, or subdural extension, especially when large. When a diagnosis of CAA is entertained, MRI should be performed with the addition of gradient echo (GRE) or susceptibility-weighted imaging (SWI). These sequences are sensitive to local magnetic field inhomogeneity and readily demonstrate small petechial hemorrhages in the cortical–subcortical regions associated with CAA (Figs. 10.1, 10.2). The petechial hemorrhages are typically less than 5mm in diameter and can sometimes be quite extensive (Fig. 10.2). Identification of these microbleeds lends specificity to a diagnosis of CAA in a patient with acute ICH. More recently, positron emission tomography (PET) imaging with the β-amyloid-binding Pittsburgh Compound B has been proposed as a potential non-invasive method for CAA detection in living subjects [1]. Other non-specific findings are frequently noted in patients with CAA, including leukoariosis and generalized brain volume loss (atrophy).