Prevalence and risk factors of cerebral microbleeds: the Rotterdam Scan Study.
BACKGROUND
Cerebral microbleeds are focal deposits of hemosiderin that can be visualized with MRI. Little is known on their prevalence in the general population and on their etiology. It has been suggested that, in analogy to spontaneous intracranial hemorrhage, the etiology of microbleeds differs according to their location in the brain, with lobar microbleeds being caused by cerebral amyloid angiopathy and deep or infratentorial microbleeds resulting from hypertension and atherosclerosis. We investigated the prevalence of and risk factors for microbleeds in the general population aged 60 years and older.


METHODS
This study is based on 1,062 persons (mean age 69.6 years) from the population-based Rotterdam Scan Study. MRI was performed at 1.5 T and included a sequence optimized to increase the conspicuity of microbleeds. We assessed the relation of APOE genotype, cardiovascular risk factors, and markers of small vessel disease to the presence and location of microbleeds with multiple logistic regression.


RESULTS
Overall prevalence of cerebral microbleeds was high and increased with age from 17.8% in persons aged 60-69 years to 38.3% in those over 80 years. APOE epsilon 4 carriers had significantly more often strictly lobar microbleeds than noncarriers. In contrast, cardiovascular risk factors and presence of lacunar infarcts and white matter lesions were associated with microbleeds in a deep or infratentorial location but not in a lobar location.


CONCLUSIONS
The prevalence of cerebral microbleeds is high. Our data support the hypothesis that strictly lobar microbleeds are related to cerebral amyloid angiopathy, whereas microbleeds in a deep or infratentorial location result from hypertensive or atherosclerotic microangiopathy.
Vernooij
M W
MW
Department of Epidemiology and Biostatistics, Erasmus MC University Medical Center, Dr. Molewaterplein 50, 3015 GE, Rotterdam, The Netherlands.
van der Lugt
A
A
Ikram
M A
MA
Wielopolski
P A
PA
Niessen
W J
WJ
Hofman
A
A
Krestin
G P
GP
Breteler
M M B
MM
D017677:Age Distribution; D000368:Aged; D000369:Aged, 80 and over; D053327:Apolipoprotein E4 / Q000235:genetics; D001921:Brain / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D016657:Cerebral Amyloid Angiopathy / Q000453:epidemiology / Q000473:pathology; D002536:Cerebral Arteries / Q000473:pathology* / Q000503:physiopathology; D002543:Cerebral Hemorrhage / Q000453:epidemiology* / Q000473:pathology* / Q000503:physiopathology; D015331:Cohort Studies; D015897:Comorbidity; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000473:pathology; D002537:Intracranial Arteriosclerosis / Q000453:epidemiology / Q000473:pathology; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008833:Microcirculation / Q000473:pathology* / Q000503:physiopathology; D008875:Middle Aged; D009426:Netherlands / Q000453:epidemiology; D011237:Predictive Value of Tests; D015995:Prevalence; D012307:Risk Factors
D053327:Apolipoprotein E4