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P1‐100: Lobar distribution of cerebral microbleeds: The Rotterdam scan study
Author(s) -
Poels Mariëlle M.F.,
Mesker Dymph J.,
Ikram M. Arfan,
Vernooij Meike W.,
Hofman Albert,
Vrooman Henri A.,
Lugt Aad,
Breteler Monique M.B.
Publication year - 2009
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2009.04.104
Subject(s) - cerebral amyloid angiopathy , medicine , dementia , population , rotterdam study , magnetic resonance imaging , asymptomatic , nuclear medicine , radiology , pathology , environmental health , disease
Background: Cerebral microbleeds (CMBs) can be detected with T2*weighted Gradient Echo sequence Magnetic Resonance Imaging (MRI) and are frequently seen in the general population. We previously reported that microbleeds in deep or infratentorial regions were associated with hypertension, whereas lobar microbleeds shared risk factors with cerebral amyloid angiopathy (CAA). We hypothesized that if lobar microbleeds in asymptomatic older persons indeed reflect amyloid angiopathy, their spatial distribution should follow the predilection sites of microbleeds in CAA. We investigated the spatial distribution of lobar microbleeds in the population based Rotterdam Scan Study. Methods: We used a three-dimensional T2* GRE sequence in 1062 participants of the population-based Rotterdam Scan Study to detect microbleeds which were defined as focal areas of very low signal intensity, smaller than 10 mm in size. Among those with lobar microbleeds (n 1⁄4 204), we assessed with Pearson’s Chi Square test whether the CMBs were equally distributed throughout the brain and with a binomial test whether the number of microbleeds per lobe were proportionate to the mean volume of the lobe on the template scan. We repeated our analysis taking clustering effects into account by adding random effects for within subject variation to our model and by weighting each microbleed as a percentage of the total number of microbleeds in each subject. Finally, we excluded all persons with additional non-lobar microbleeds and reran our analyses in persons with strictly lobar microbleeds (n 1⁄4 146). Results: In total, we counted 1,010 lobar microbleeds. The median number of lobar microbleeds was 1 (range 1-114). Compared with the expected distribution of microbleeds based on the volume of the lobes, we found that lobar as well as strictly lobar cerebral microbleeds occurred significantly more often in the temporal lobe (p-value < 0.05). Analysis accounting for the possibility of clustering confirmed our findings. Conclusions: In the general population, lobar microbleeds show a predilection for the posterior brain regions, particularly the temporal lobes. This corroborates the presumed association of lobar microbleeds with CAA in the general population.

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