Cerebral Cortical Microinfarcts on Magnetic Resonance Imaging and Their Association With Cognition in Cerebral Amyloid Angiopathy.

Background and Purpose- We aimed to explore the association between presence of cerebral cortical microinfarcts (CMIs) on magnetic resonance imaging and other small-vessel disease neuroimaging biomarkers in cerebral amyloid angiopathy (CAA) and to analyze the role of CMIs on individual cognitive domains and dementia conversion. Methods- Participants were recruited from an ongoing longitudinal research cohort of eligible CAA patients between March 2006 and October 2016. A total of 102 cases were included in the analysis that assessed the relationship of cortical CMIs to CAA neuroimaging markers. Ninety-five subjects had neuropsychological tests conducted within 1 month of magnetic resonance imaging scanning. Seventy-five nondemented CAA patients had cognitive evaluation data available during follow-up. Results- Among 102 patients enrolled, 40 patients had CMIs (39%) on magnetic resonance imaging. CMIs were uniformly distributed throughout the cortex without regional predilection ( P=0.971). The presence of CMIs was associated with lower total brain volume (odds ratio, 0.85; 95% CI, 0.74-0.98; P=0.025) and presence of cortical superficial siderosis (odds ratio, 2.66; 95% CI, 1.10-6.39; P=0.029). In 95 subjects with neuropsychological tests, presence of CMIs was associated with impaired executive function (ß, -0.23; 95% CI, -0.44 to -0.02; P=0.036) and processing speed (ß, -0.24; 95% CI, -0.45 to -0.04; P=0.020). Patients with CMIs had a higher cumulative dementia incidence compared with patients without CMIs ( P=0.043), whereas only baseline total brain volume (hazard ratio, 0.76; 95% CI, 0.62-0.92; P=0.006) independently predicted dementia conversion. Conclusions- Magnetic resonance imaging-detected CMIs in CAA correlated with greater overall disease burden. The presence of CMIs was associated with worse cognitive performance, whereas only total brain atrophy independently predicted dementia conversion.

Evolution of DWI lesions in cerebral amyloid angiopathy: Evidence for ischemia.

OBJECTIVE: To address the pathophysiologic nature of small diffusion-weighted imaging (DWI) lesions in patients with cerebral amyloid angiopathy (CAA) who underwent serial MRI. Specifically, we tested (1) whether DWI lesions occurred preferentially in individuals with prior DWI lesions, (2) the cross-sectional association with chronic cortical cerebral microinfarcts (CMIs), and (3) the evolution of DWI lesions over time. METHODS: Patients with probable CAA (n = 79) who underwent at least 2 MRI sessions were included. DWI lesions were assessed at each available time point. Lesion appearance and characteristics were assessed on available structural follow-up images. Presence and burden of other neuroimaging markers of small vessel disease (white matter hyperintensities, cerebral microbleeds, cortical superficial siderosis, and chronic cortical CMIs) were assessed as well. RESULTS: Among 221 DWI scans (79 patients with 2 DWI scans; 40 with ≥3), 60 DWI lesions were found in 28 patients. Patients with DWI lesions at baseline were not more likely to have additional DWI lesions on follow-up compared to patients without DWI lesions at baseline. DWI lesions were associated with chronic cortical CMIs and cortical superficial siderosis, but not with other markers. For 39/60 DWI lesions, >1 MRI sequence was available at follow-up to determine lesion evolution. Twenty-four (62%) were demarcated as chronic lesions on follow-up MRI. Five appeared as cavitations, 18 as noncavitated infarcts, and 1 underwent hemorrhagic transformation. CONCLUSIONS: Based on their neuroimaging signature as well as their association with chronic cortical CMIs, DWI lesions appear to have an ischemic origin and represent one part of the CMI spectrum.