Abstract 50: Interrelationship Between Lacunes and Cortical Microinfarcts in Cerebral Amyloid Angiopathy

Abstract

Background: Cerebral amyloid angiopathy (CAA) is known for its hemorrhagic manifestations, but ischemic features of the disease are also recognized such as white matter hyperintensities (WMH). We aimed to investigate the interrelationship between two emerging ischemic markers related to CAA: lacunes and cortical microinfarcts (CMI). Methods: CMI were scored on MRIs using high resolution FLAIR, double inversion recovery and MEMPRAGE sequences, in prospectively enrolled patients with CAA. The presence, number, and topography of lacunes (deep vs. subcortical), cerebral microbleeds (CMB), cortical superficial siderosis (cSS), and enlarged perivascular spaces (EPVS) were identified. FreeSurfe r was used for volumetric analyses. The relationship of CMI and lacunes as well as the association of these lesions with other CAA-related markers were analyzed. Results: The cohort consisted of 122 nondemented probable CAA patients (mean age, 69.4±7.6 years, 73% men). Lacunes were present in 31 (25.4%) of the patients and all but 1 were located in subcortical as opposed to deep brain regions. Lacunes were not associated with age, sex, or vascular risk factors. CMI were found in 35 patients (28.7%). CMI were more common in patients with lacunes compared to patients without lacunes (51.6% vs. 20.9%, p=0.002) and this association remained significant in a multivariable model adjusting for age, sex and hypertension (odds ratio: 4.2, 95% CI: 1.75-10, p=0.001). WMH volume, EPVS, WM volume, cortical thickness, and hemorrhagic markers did not differ between patients with or without lacunes (p>0.2 for all comparisons). CMI did not correlate with these markers except showing a positive association with presence/extent of cSS. Conclusion: Lacunes and CMI were common in CAA, and lacunes were more commonly found in subcortical WM as opposed to deep gray structures. Our study shows that CMI are more likely to occur in probable CAA patients with lacunes than without lacunes, suggesting that these two lesion types may be part of a common spectrum of small CAA-related ischemic infarcts. These pathologies did not correlate with markers of more widespread damage, however, suggesting that the mechanism for CAA-related infarcts is distinct from other more widespread effects of CAA.