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SAGE Publications, International Journal of Stroke, SA100(9), p. 48-54, 2014

DOI: 10.1111/ijs.12275

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Cognitive Performance after Stroke – The Framingham Heart Study

This paper is available in a repository.
This paper is available in a repository.

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Abstract

Background Individuals with a high risk of stroke are also more prone to cognitive impairment perhaps because of concomitant vascular risk factors. In addition, clinical stroke increases the risk of subsequent dementia. Nevertheless, the relationship between clinical stroke and subsequent cognitive function in initially nondemented individuals remains less clear as most prior studies examined case series without controls. Aims To specify among nondemented individuals the cognitive domains affected by clinical stroke, independently of vascular risk factors and prestroke cognition. Methods One hundred thirty-two Framingham study participants (mean age = 77 ± 9 years, 54% women) with prospectively validated initial strokes, as well as age- and gender-matched controls, underwent identical cognitive evaluations ∼six-months after the stroke. Linear regression models were used to assess the differences in cognitive scores between stroke cases and controls adjusting for prestroke cognitive function as assessed by Mini-Mental State Examination scores, and with and without adjustment for vascular risk factors. Results Adjusting for prestroke cognition and vascular risk factors, persons with stroke had poorer cognitive function in the domains of immediate recall of logical and visual memories (β = −1·27 ± 0·60, P = 0·035; β = −1·03 ± 0·47, P = 0·028, respectively), verbal learning (paired associate test; β = −1·31 ± 0·57, P = 0·023), language (Boston naming test; β = −0·27 ± 0·08, P = 0·002), executive function (digit span backward; β = −0·53 ± 0·21, P = 0·015), and visuospatial and motor skills (block design; β = −3·02 ± 1·06, P = 0·005). Conclusions Clinical stroke is associated with subsequent poorer performance in multiple cognitive domains. This association cannot be entirely explained by the individual's cognitive function prior to stroke or by concomitant vascular risk factor levels.