Distributional Impact of Brain Microbleeds on Global Cognitive Function in Adults Without Neurological Disorder

Y. Yakushiji, T. Noguchi, M. Hara, M. Nishihara, M. Eriguchi, Y. Nanri, M. Nishiyama, T. Hirotsu, J. Nakajima, Y. Kuroda, H. Hara
2012 Stroke  
and Purpose-Brain microbleeds (MBs) are considered to be associated with cognitive decline and can be pathologically and topographically classified as cerebral amyloid angiopathy-related (located in lobar regions) and hypertensive microangiopathy-related (located in deep regions). We examined whether different effects on global cognitive function might be seen with different distributions of MBs. Methods-A total of 1279 adults without neurological disorders were studied prospectively. Subjects
more » ... ectively. Subjects were divided into 4 groups: without-MBs group; lobar group; deep group; and with in both areas (diffuse group). The Mini-Mental State Examination was administered to determine global cognitive functions, with scores Ͻ27 regarded as subnormal. Results-MBs were detected in 98 subjects (8%): 36 subjects (3%) classified as lobar group, 48 subjects (4%) as deep group, and 14 subjects (1%) as diffuse group. Subnormal scores were found in 76 subjects (5.9%), associated with age, education, hypertension, severe white matter hyperintensities, and distribution and number of MBs. In the final model of logistic regression analysis, the deep group (OR, 2.79; 95% CI, 1.14 -6.79) was associated with subnormal scores, whereas the lobar group (OR, 0.77; 95% CI, 0.17-3.44) was not. Trend for the diffuse group did not reach the level of significance (OR, 5.01; 95% CI, 0.88 -28.41). These trends were also seen in analysis using another cut-off point for subnormal score. Scores for total Mini-Mental State Examination and attention and calculation were significantly lower in the deep group and the diffuse groups compared with the without-MBs group. Conclusions-This Japanese cross-sectional study demonstrated that MB-related global cognitive dysfunction seems to occur based on hypertensive pathogenesis rather than on cerebral amyloid angiopathy. (Stroke. 2012;43:1800-1805.)
doi:10.1161/strokeaha.111.647065 pmid:22581820 fatcat:il34wntyoneybmag4tu7dzugui