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Of the metals that are commonly present in the human brain, it is considered that only iron in the form of ferritin and hemosiderin is present in sufficient quantities and appropriate oxidation state to be visualized by magnetic resonance imaging (MRI). Histology has shown that cerebral microbleeds (CMBs) contain hemosiderin deposits, a paramagnetic substance. In attempts to quantify the actual susceptibility distribution, many different models have been proposed, which relate measurable MRI effects to the underlying susceptibility distribution. However, for the detection of CMBs it is probably sufficient to use qualitative techniques with a high sensitivity to magnetic field inhomogeneities to provide information on the location and approximate size of the CMB. This chapter describes some possible technical developments to discriminate between some of the different origins of signal loss. The introduction of higher-field scanners and the development of new sequences can provide increased sensitivity for the detection of CMBs.
This chapter summarizes the current knowledge on prevalence and characteristics of cerebral microbleeds (CMBs) in normal individuals. The most solid knowledge on CMBs comes from the population-based studies, in particular those that have included higher age groups and have used a sensitive technique to detect CMBs. The four population-based studies with reported findings on CMBs in normal individuals are the Austrian Stroke Prevention Study, the Framingham Study, the Age Gene/Environment Susceptibility (AGES)-Reykjavik study (AGES-R) and the Rotterdam Scan Study. A pioneering study from Japan studied the prevalence of CMBs in 450 neurologically healthy Japanese adults with a mean age of 52.9 years. The overall incidence was 3.1% (14/450), and lesions detected were closely related to hypertension and heavy cigarette smoking. Patterns of risk factors and comorbidities are different between regions, and one can assume that such factors should also affect prevalence rates of CMBs.
Stroke is a leading cause of death and disability throughout the world. About one in three symptomatic strokes are due to disease of small perforating arteries; however, most effective interventions are targeted at disease of large arteries. The underlying mechanisms and treatment of small vessel disease remain poorly understood. Microbleeds have emerged as a critical imaging marker of small vessel disease, being found in all types of stroke. With increasing evidence that microbleeds are caused by hypertensive arteriopathy and cerebral amyloid angiopathy, they are likely to play a strong future role in increasing our understanding of the causes of small vessel disease and the potential link between cerebrovascular disease and neurodegeneration. Cerebral Microbleeds summarizes our current knowledge, bringing together expert research from global authorities in the field. This authoritative and systematic text will be of interest to all clinical researchers and physicians in the fields of stroke and cognitive impairment.
This chapter provides an overview of the prevalence and associations, temporal evolution and prognostic significance of cerebral microbleeds (CMBs) in patients with cerebrovascular diseases. The spatial distribution of microbleeds, as markers of small vessel microhemorrhagic or microaneurysmal lesions, may be of particular interest in attempts to understand the causes of macroscopic intracerebral hemorrhage (ICH) in life. Cerebral amyloid angiopathy is an important cause of primary ICH, particularly of lobar location. Chronic hypertension has been repeatedly identified as a strong influence on the frequency and extent of CMBs, in patients with established stroke as well as in healthy subjects without stroke. Hypertension is an important risk factor for CMBs. As CMBs reflect the bleeding tendency of the brain through fragile microvascular walls, interest has increased in utilizing CMBs in risk stratification of hemorrhagic complications for patients with antithrombotic treatment.