Advances in Vascular Cognitive Impairment

Abstract

Vascular cognitive impairment (VCI) has continued to evolve over the past year. Much of the data has been confirmatory with further work on risk factors, silent strokes, leukoaraiosis and lesion volume and location. The importance of the interaction between cerebrovascular disease and other causes of cognitive impairment, most importantly Alzheimer disease (AD) remains a prominent theme. The natural history of VCI remains uncertain and further data on the rate of progression and factors affecting this are presented. It increasingly seems that the rate of progression in well-defined cases is low with no progression over 1 year in 1 study. Interestingly, a novel study from Toronto suggested that steal may be an etiologic mechanism. New trial data have been scanty but of note 1 long trial of aspirin was negative. Silent strokes are the most common form of stroke.1 In 1998 in the United States it was estimated that there were about 9 million silent infarcts and 2 million silent hemorrhages. Cerebral infarcts are an important cause of dementia; however, there is controversy regarding the role of silent or asymptomatic infarcts, infarct size and location, and vascular risk factors.2 Troncoso et al2 report autopsy findings from the Baltimore Longitudinal Aging Study among 122 men and 57 women of whom 92% were white, had 17.5 years of education, and a mean age at death of 86.9 years. The odds of dementia were increased by both asymptomatic and symptomatic infarcts; however, dementia was not increased by risk factors for stroke in the absence of an infarct. Number but not size of hemispheral infarct was important, whereas subcortical infarcts conferred no increased risk of dementia. Macroscopic and microscopic infarcts contributed equally to dementia risk, and hemispheral infarcts, whether silent or clinically manifest, alone or in conjunction with AD pathology accounted for …