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Review
. 2010 Aug;67(2):484-93; discussion 493-4.
doi: 10.1227/01.NEU.0000371730.11404.36.

A review of carotid atherosclerosis and vascular cognitive decline: a new understanding of the keys to symptomology

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Review

A review of carotid atherosclerosis and vascular cognitive decline: a new understanding of the keys to symptomology

Robert J Dempsey et al. Neurosurgery. 2010 Aug.

Abstract

This review encourages the reader to consider cerebral vascular disease beyond the traditional clinical end points of major motor and speech strokes and to consider the possible impact of embolic cerebral vascular disease on vascular cognitive decline. This article examines the issue of "silent" strokes in the relationship between the structural stability of atherosclerotic carotid plaque and the development of nonmotor symptomatology, including cognitive decline. It addresses the question of the role of carotid emboli in silent stroke and their cognitive sequelae. In a study of endarterectomy patients, we relate plaque elasticity and its development of mechanical strain features and thinning of stabilizing fibrous cap at the point of these mechanical strain features. The possibility that microemboli from such mechanically unstable carotid plaques could contribute to silent strokes led to a study of cognitive function in such patients. A linear relationship between the process of mechanically unstable areas of carotid plaques and cognitive decline suggests a contributory role for such a process in silent strokes.

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Figures

Figure 1
Figure 1
Cross section of carotid atherosclerosis showing fibrous cap adjacent to the lumen. L = Lumen FC = Fibrous Cap PC = Plaque
Figure 2
Figure 2
Gene ontological analysis of the biological functions of transcripts more abundantly expressed in the symptomatic plaques showed a neoplastic phenotype.
Figure 3
Figure 3
Increased expression of genes that control angiogenesis in symptomatic plaque samples.
Figure 4
Figure 4
Age adjusted standard scores demonstrating a pattern of generally depressed mental status across tested cognitive domains. Relationships were in the similar direction, but weaker, across tests of visual perception, language and attention r’s from −.37 to −.31).
Figure 5
Figure 5
(a) B-mode gray scale ultrasound image, (b) 2-D elastogram, (c) B-mode with colorflow of an in-vivo carotid artery with plaque visible near the wall of the vessel close to the bifurcation. Note also the presence of turbulent flow around this region. Elastographically strain here appears as a more friable or more likely to fracture region and is depicted as the brighter region.
Figure 6
Figure 6
Plot of the RBANS total score versus maximum accumulated frame strain (single observer measurement) over a cardiac cycle.

References

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