Introduction: Small hyperintense diffusion-weighted imaging (DWI) lesions are frequent neuroimaging findings in patients with cerebral amyloid angiopathy (CAA). Despite their high occurrence, little is known about the clinical impact of these lesions as well as their evolution over time and potential underlying etiology. Although it is believed that DWI-bright lesions represent acute microinfarcts, it has also been suggested that they are precursors of microbleeds. In this study we assessed DWI lesions in a cohort of CAA patients that underwent multiple imaging sessions. Specifically, we addressed the pathophysiologic nature of DWI lesions by evaluating their appearance on follow-up MRI.
Methods: Patients (n=79) with probable CAA, as assessed by the Boston criteria, who underwent at least two DWI scans >2 months apart (>2 weeks post-ICH), were included in the study. One experienced neuroradiologist assessed presence and number of DWI lesions at each available time-point. Lesions had to be hyperintense on DWI, hypointense on ADC, and isointense on GRE. Next, on available follow-up images (FLAIR, T1, and GRE scans), lesion visibility and imaging characteristics were assessed by two experienced raters. All ratings were performed on 1.5 T MRI scans.
Results: A total number of 221 DWI scans were assessed for DWI lesions (39 patients had 2 DWI scans; 40 had ≥3). In total, 57 DWI lesions were found in this dataset (37 in white matter; 16 in grey matter; 4 in cerebellum). For 36/57 lesions >1 imaging sequence was available at follow-up to determine lesion appearance. Twenty-two/36 DWI lesions (61%) were visible on follow-up MRI. Five appeared as lacunar infarcts (of which 4 were located in white matter), 16 were visible as signal change on T1 or FLAIR sequences. Only a single DWI lesion showed evidence of hemosiderin deposition on follow-up, compatible with hemorrhagic transformation / microbleed.
Conclusions: DWI lesions are common neuroimaging findings in patients with probable CAA. More than 60% of the observed DWI lesions evolve into chronic lesions, but the minority shows cavitation. Their neuroimaging signature strongly suggests that these lesions have an ischemic pathophysiologic nature. We found only one lesion that underwent hemorrhagic transformation.