Table of contents
Does Stroke Contribute to Racial Differences in Cognitive Decline?
Deborah A. Levine, MD, MPH, deblevin at umich.edu Mohammed Kabeto, MS, Kenneth M. Langa, MD, PhD, Lynda D. Lisabeth, PhD, Mary A.M. Rogers, PhD and Andrzej T. Galecki, MD, PhD
From the Department of Internal Medicine (D.A.L., M.K., K.M.L., M.A.M.R., A.T.G.), Stroke Program (D.A.L., L.D.L.), Institute for Social Research (K.M.L.), Department of Epidemiology (L.D.L.), Department of Biostatistics (A.T.G.), University of Michigan, Ann Arbor; and Veterans Affairs Center for Clinical Management Research, Ann Arbor, MI (D.A.L., K.M.L.).
Presented in part at the International Stroke Conference of the American Heart Association, San Diego, CA, February 12–14, 2014.
Background and Purpose—It is unknown whether blacks’ elevated risk of dementia is because of racial differences in acute stroke, the impact of stroke on cognitive health, or other factors. We investigated whether racial differences in cognitive decline are explained by differences in the frequency or impact of incident stroke between blacks and whites, controlling for baseline cognition.
Methods—Among 4908 black and white participants aged ≥65 years free of stroke and cognitive impairment in the nationally representative Health and Retirement Study with linked Medicare data (1998–2010), we examined longitudinal changes in global cognition (modified version of the Telephone Interview for Cognitive Status) by race, before and after adjusting for time-dependent incident stroke followed by a race-by-incident stroke interaction term, using linear mixed-effects models that included fixed effects of participant demographics, clinical factors, and cognition, and random effects for intercept and slope for time.
Results—We identified 34 of 453 (7.5%) blacks and 300 of 4455 (6.7%) whites with incident stroke over a mean (SD) of 4.1 (1.9) years of follow-up (P=0.53). Blacks had greater cognitive decline than whites (adjusted difference in modified version of the Telephone Interview for Cognitive Status score, 1.47 points; 95% confidence interval, 1.21 to 1.73 points). With further adjustment for cumulative incidence of stroke, the black–white difference in cognitive decline persisted. Incident stroke was associated with a decrease in global cognition (1.21 points; P<0.001) corresponding to ≈7.9 years of cognitive aging. The effect of incident stroke on cognition did not statistically differ by race (P=0.52).
Conclusions—In this population-based cohort of older adults, incident stroke did not explain black–white differences in cognitive decline or impact cognition differently by race.
Trajectory of Cognitive Decline After Incident Stroke (no mention of vitamin D)
JAMA. 2015;314(1):41-51. doi:10.1001/jama.2015.6968.
Deborah A. Levine, MD, MPH1,2,3,4; Andrzej T. Galecki, MD, PhD1,5; Kenneth M. Langa, MD, PhD1,2,3,6; Frederick W. Unverzagt, PhD7; Mohammed U. Kabeto, MS1,2; Bruno Giordani, PhD8; Virginia G. Wadley, PhD9
Importance Cognitive decline is a major cause of disability in stroke survivors. The magnitude of survivors’ cognitive changes after stroke is uncertain.
Objective To measure changes in cognitive function among survivors of incident stroke, controlling for their prestroke cognitive trajectories.
Design, Setting, and Participants Prospective study of 23 572 participants 45 years or older without baseline cognitive impairment from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort, residing in the continental United States, enrolled 2003-2007 and followed up through March 31, 2013. Over a median follow-up of 6.1 years (interquartile range, 5.0-7.1 years), 515 participants survived expert-adjudicated incident stroke and 23 057 remained stroke free.
Exposure Time-dependent incident stroke.
Main Outcomes and Measures The primary outcome was change in global cognition (Six-Item Screener SIS, range, 0-6). Secondary outcomes were change in new learning (Consortium to Establish a Registry for Alzheimer Disease Word-List Learning; range, 0-30), verbal memory (Word-List Delayed Recall; range, 0-10), and executive function (Animal Fluency Test; range, ≥0), and cognitive impairment (SIS score <5 [impaired] vs ≥5 [unimpaired]). For all tests, higher scores indicate better performance.
Results Stroke was associated with acute decline in global cognition (0.10 points [95% CI, 0.04 to 0.17]), new learning (1.80 points [95% CI, 0.73 to 2.86]), and verbal memory (0.60 points [95% CI, 0.13 to 1.07]). Participants with stroke, compared with those without stroke, demonstrated faster declines in global cognition (0.06 points per year faster [95% CI, 0.03 to 0.08]) and executive function (0.63 points per year faster [95% CI, 0.12 to 1.15]), but not in new learning and verbal memory, compared with prestroke slopes. Among survivors, the difference in risk of cognitive impairment acutely after stroke, compared with immediately before stroke, was not statistically significant (odds ratio, 1.32 [95% CI, 0.95 to 1.83]; P = .10); however, there was a significantly faster poststroke rate of incident cognitive impairment compared with the prestroke rate (odds ratio, 1.23 per year [95% CI, 1.10 to 1.38]; P < .001). For a 70-year-old black woman with average values for all covariates at baseline, stroke at year 3 was associated with greater incident cognitive impairment: absolute difference of 4.0% (95% CI, −1.2% to 9.2%) at year 3 and 12.4% (95% CI, 7.7% to 17.1%) at year 6.
Conclusions and Relevance Incident stroke was associated with an acute decline in cognitive function and also accelerated and persistent cognitive decline over 6 years.
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Stroke, Cognitive Decline and Vascular Dementia: The Silent Epidemic of the 21st Century - 2003
Neuroepidemiology 2003;22:161–164, DOI: 10.1159/000069885
Gustavo C. Roma´n, Editor-in-Chief - Editorial
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Strokes ==> decrease Vitamin D levels
Low vitamin D ==> reduced cognition
Suspect that stroke ==> reduced cognition is due to lowered vitamin D