A significant spatial and temporal association exists between cortical microinfarcts (CMIs) and cortical superficial siderosis (cSS) in cerebral amyloid angiopathy (CAA).
Regions of the cortex affected by cSS exhibit markedly higher densities of CMIs, supporting the hypothesis that hemosiderin deposits from cSS may contribute to local ischemic injury.
Baseline cSS volume independently predicts the development of new cortical microinfarcts over 24 months, whereas baseline CMI burden does not predict cSS progression.
These findings identify potential mechanistic pathways linking hemorrhagic and ischemic brain injuries in CAA and suggest new targets for preventing cortical injury.
