Microembolism, silent brain infarcts and dementia
Introduction
Age-related cognitive decline and dementia are now more prevalent than ever. One can reasonably predict that this issue will increase further due to the growing life expectancy of the general population. It is crucial, however, to ensure that gains in years of life will be matched by equal gains in the quality of life. At present, approximately 1% of 65-year-olds and at least 30% of 90-year-olds have a dementia disorder [1], with a large toll on the independence and quality of life of patients and caregivers.
Vascular dementia (VaD) is considered the second most common cause of dementia and, together with Alzheimer's disease (AD), represents the majority of all cases of dementia [2]. VaD predominantly affects patients with cardiovascular risk factors e.g., hypertension, diabetes mellitus, hyperlipidemia, smoking, etc. However, the same risk factors are also found in patients diagnosed as having AD [3]. Significant therapies are still missing and much effort is therefore being devoted to the prevention of dementia. Rather than acting separately, it is now believed that AD and VaD are frequently present in the same brain. The so-called mixed dementia occurs more often than was previously realized [4] particularly in elderly people with cardiovascular risk factors who present with slow progressive cognitive decline. The clear cut border discriminating VaD from AD is blurred in reality [5] and challenges our attempts to understand, cure or prevent dementia.
Conceptually well differentiated from AD, the cognitive deterioration in VaD is thought to be the result of cerebral ischemia secondary to vascular pathologies. While acute and focal ischemia produce relatively well recognized clinical pictures (e.g. symptomatic stroke, lacunar stroke, Binswanger's disease), it is the more chronic and diffuse aspects of brain infarction that have been the focus of recent attention and the purpose of this review.
We have reviewed recent published clinical evidence on the association of cerebral microemboli causing silent brain ischemia as contributors to cognitive decline and dementia. The sources of microemboli are manifold and mainly divided between cardiac and vascular origins. Here we have focused on specific sources of microemboli—especially atrial fibrillation (AF) and atherosclerotic aortic and carotid disease [6], [7]. Microemboli are associated with structural brain changes and with cognitive decline [8]. Finally, the role of transcranial Doppler (TCD) as an objective tool for detecting and quantifying microemboli is discussed.
Section snippets
Atherosclerosis
White matter hyperintense lesions (WMHL) are a common finding on neuroimaging among the elderly population and were previously associated with neurological morbidity. However, it should be emphasized that WMHL is a descriptive term as a radiological entity which was not recognized prior to the development of CT and MRI, although cognitive impairment as a manifestation of white matter pathology has been described by Binswanger many years ago [9]. This is an unusual situation in which radiology
Conclusions
The distinction between primary and secondary degenerative brain disorder causing cognitive impairment is more blurred than ever. As both silent cerebral infarction and neurodegenerative processes play a role in cognitive decline, their interactions and cohabitation remain to be better understood and unraveled. More prospective large clinical trials are mandatory in order to shed further light on the question of causality or association between microvascular changes, emboli, chronic silent
Conflict of interest statement
None.
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