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(Stroke. 2008;39:279.)
© 2008 American Heart Association, Inc.
Advances in Stroke 2007 |
From the Center for Stroke Research, Department of Neurology and Rehabilitation (P.B.G.), University of Illinois College of Medicine at Chicago, Ill; and the Royal Free Hospital, Department of Neurology (J.V.B.), London, UK.
Correspondence to Philip B. Gorelick, MD, MPH, FACP, John S. Garvin Professor and Head, Director, Center for Stroke Research, Department of Neurology and Rehabilitation, University of Illinois College of Medicine at Chicago, 912 S. Wood Street Room 855N, Chicago, Illinois 60612. E-mail pgorelic@uic.edu
Key Words: neuroimaging risk factors treatment vascular cognitive impairment
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Vascular cognitive impairment (VCI) remains a challenge of integrating what we know with evaluating what we do to catalyze progress.1 Hachinski has suggested that we optimize knowledge acquisition and application in stroke and VCI by "The Triple T Approach" of transdisciplinary, translational, and transactional interchanges.1 Our understanding of VCI continues to evolve and cannot be taken in isolation of Alzheimer disease (AD) as important overlap and potential synergy may exist for the two disorders. In relation to VCI, select studies published in 2007 have shown that: (1) Knowledge of post-stroke cognitive impairment and its long-term development is poor as illustrated by the nonlinear time course of memory dysfunction after stroke2,3; (2) A history of stroke symptoms without a history of stroke or TIA (so-called "whispering strokes") is associated with cognitive impairment which is increased with the occurrence of each additional modifiable cardiovascular risk factor4; and (3) For cognitive impairment, no dementia (CIND), and mild cognitive impairment (MCI), a history of previous stroke may increase the risk of dementia.5 In this update we review advances in VCI that took place in 2007.
Neuropathology
Based on 148 autopsy subjects of the Rush Memory and Aging Project, Schneider et al reported that after controlling for cortical infarcts and AD pathology, subcortical infarcts increased the odds of dementia by almost 4 times, reduced cognitive function by more than a third of a unit (P=0.03), were associated with lower episodic memory, semantic, and working memory (P
0.05), and interacted with AD
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