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  • Title: Cerebral microbleeds: a review.
    Author: Loitfelder M, Seiler S, Schwingenschuh P, Schmidt R.
    Journal: Panminerva Med; 2012 Sep; 54(3):149-60. PubMed ID: 22801432.
    Abstract:
    Cerebral microbleeds (CMBs) are frequent findings in MRI scans of elderly subjects. Depending on the MRI protocols applied 4.7% to 24.4% of community-based subjects show incidental CMBs. The rates reported for various types of ischemic strokes and intracerebral hemorrhages vary between 19.4% and 68.5%. Most studies also demonstrated CMBs in approximately one third of Alzheimer cases. A lobar distribution of CMBs is considered to relate to cerebral amyloid angiopathy, while CMBs located in the basal ganglia or in infratentorial brain regions are thought to relate to hypertensive vasculopathy. Besides age, hypertension, diabetes mellitus, and low serum cholesterol have so far been identified as risk factors for CMBs. Presence of an APOE ε4 allele is the only genetic factor that was consistently shown to increase the risk for CMB development. There are only few longitudinal studies on the predictive value of CMBs. For incident ischemic strokes and intracerebral hemorrhages hazard ratios of 4.48 and 50.2 have been reported. CMBs also doubled the risk for conversion to dementia in MCI patients, and there are indications for CMBs being possible predictors of increased mortality. Given the small number of longitudinal investigations with often small sample sizes the role of CMBs as predictors of disease needs to be further elucidated. CMBs were significantly more common in warfarin-treated stroke patients who developed intracerebral hemorrhages (ICH). These data are cross-sectional. They do not provide enough evidence to consider CMBs as a contraindication for antithrombotic agents in primary and secondary stroke prevention. CMBs are likely to unfavourably affect cognitive functioning. It remains to be determined if direct lesion-related effects are responsible for this finding or if CMBs are sole markers of more extensive tissue damage in the wake of cerebral small vessel disease leading to widespread visible but also non-visible tissue destruction with a high likelihood for cognitive consequences.
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