Background: In patients with symptomatic cerebral amyloid angiopathy (CAA), cerebrovascular reactivity to visual stimuli is reduced. Lobar microbleeds are a diagnostic hallmark of CAA, but are also highly prevalent in asymptomatic individuals. Recent data suggest that the latter group might have CAA. Objective: We investigated whether cerebrovascular reactivity is impaired in asymptomatic individuals with lobar microbleeds.
Methods: From the population-based Rotterdam Study, we invited 35 participants with lobar microbleeds and 15 age-matched controls (all≥55 years) for functional MRI (fMRI) as part of the Early Detection of Angiopathy Network (EDAN) Study. Cerebrovascular reactivity parameters (i.e., amplitude and time to peak responses) were assessed in response to visual stimulation using fMRI. Student's t-test and linear regression were used to compare fMRI parameters in participants with and without microbleeds.
Results: Amplitude and time to peak responses did not differ between participants with and without microbleeds (respectively, p=0.179 and p=0.555). Participants with microbleeds had slightly higher amplitude responses compared to participants without microbleeds. After excluding individuals with mixed microbleeds (i.e., lobar and non-lobar microbleeds), we found no significant difference in cerebrovascular reactivity for persons with a single microbleed or multiple microbleeds compared to persons without microbleeds.
Conclusions: In the general population, lobar microbleeds may not relate to impaired cerebrovascular reactivity. In asymptomatic individuals, lobar microbleeds may either reflect less advanced CAA pathology insufficient to cause functional vascular impairment, or reflect vascular pathology other than CAA.

, , ,,
Journal of Alzheimer's Disease
Department of Epidemiology

Akoudad, S., Gurol, M.E. (M. Edip), Fotiadis, P. (Panagiotis), Koudstaal, P., Hofman, A., Ikram, A., … Vernooij, M. (2016). Cerebral Microbleeds and Cerebrovascular Reactivity in the General Population: The EDAN Study. Journal of Alzheimer's Disease, 53(2), 497–503. doi:10.3233/JAD-151130