Longitudinal Effect of Stroke on Cognition: A Systematic Review

Background Stroke is associated with an increased risk of dementia; however, the impact of stroke on cognition has been found to be variable, such that stroke survivors can show decline, remain stable, or revert to baseline cognitive functioning. Knowing the natural history of cognitive impairment after stroke is important for intervention. The aim of this systematic review is to investigate the longitudinal course of cognitive function in stroke survivors. Methods and Results Three electronic databases (Medline, Embase, PsycINFO) were searched using OvidSP from inception to July 15, 2016. Longitudinal studies with ≥2 time points of cognitive assessment after stroke were included. In total, 5952 articles were retrieved and 14 were included. There was a trend toward significant deterioration in cognitive test scores in stroke survivors (8 studies). Cognitive stability (3 studies) and improvement (3 studies) were also demonstrated, although follow‐up time tended to be shorter in these studies. Variables associated with impairment included age, ethnicity, premorbid cognitive performance, depression, stroke location, and history of previous stroke. Associations with APOE*E4 (apolipoprotein E with the E4 allele) allele status and sex were mixed. Conclusions Stroke is associated with an increased risk of cognitive decline, but cognitive decline is not a consequence. Factors associated with decline, such as sociodemographic status, health‐related comorbidity, stroke history, and clinical features could be used in models to predict future risk of dementia after stroke. A risk model approach could identify patients at greatest risk for timely intervention to reduce the frequency or delay the onset of poststroke cognitive impairment and dementia.

Second round of data collection: baseline assessment and at 1, 2, and 3 weeks after the baseline assessment in each individual.

NOT REPORTED
Ben Assayag 2015 7 Tel Aviv Brain Acute Stroke Cohort (TOBASCO) Study (n -298) Mean age 66.7+/-9.6 years 62.4% male (n = 186) Mean education 13.2 (SD 3.7) years Baseline MoCA and NeuroTrax computerised cognitive testing and then repeated at 6, 12 and 24 months following the event. The average of the 6 index scores (memory, executive functions, visuospatial perception, verbal function, attention and motor skills) was computed as the global cognitive score.  Interactions between time and stroke (mean differences in cognitive function) between those with and those without stroke Cognitive decline increased significantly after stroke relative to before stroke.
Cognitive decline increased 1.9 fold after incident stroke with cognitive function predicting mortality even after adjusting for stroke, demographic and health related factors.
Kohler 2012  APOE e4 carriers demonstrated a non-significantly lowered risk for MMSE decline. APOE e4 associated with declines in info processing speed and small declines for immediate and delayed recall. Of the 53 stroke patients -(n=17) had the e4 allele for APOE, (n=36) did not. Stroke patients without ApoE e4 had the lowest changes in MMSE (-1.6 points). Stroke patients with e4 showed greater declines in info processing speed (-2.0 points). Reitz 2006 5 NOT REPORTED NOT REPORTED Memory declined significantly over time (β= -1.6, p=0.005), abstract/visuospatial and language performance remained stable. A history of stroke was associated with more rapid decline in memory performance over time (β=-3.6, p=0.04). There was no relation between stroke and decline in abstract/visuospatial or language performance.
Memory and abstract/visuospatial function declined at a faster rate in men or persons who lacked the APOEe4 allele with stroke compared to women or APOEe4 carriers. This remain unchanged after adjusting for age, education, ethnic group, BMI< hypertension, heart disease, diabetes and smoking.
The association between stroke and decline in memory performance was strongest for men and for persons without an APOE4 allele. A significant association between stroke and decline in abstract/visuospatial performance was also observed for persons without the APOE-e4 allele. Univariate predictors of cognitive decline 24 months from stroke include: age greater than or equal to 75, education <12 years, white matter lesion score, Modified Rankin score 6 months after stroke, MoCA score at hospital admission, MoCA score 6 months after stroke, Berg Balance Scale 6 months after stroke (<50), the Timed Up and Go test score 6 months after stroke (>12 seconds), number of correct answers during dual-task 6 months after stroke (<15). Multivariate predictors include age greater than or equal to 75 years, TUG score (> 12secs) 6 months after stroke, MoCA score 6 months after stroke Balance and gait are significant risk markers for cognitive status and impaired cognitive recovery after mild stroke or TIA Univariate predictors of cognitive decline 24 months from stroke include: age greater or equal to 75 years, education <12 years, ischaemic heart disease, hypertension, white matter lesion score, MoCA score at hospital admission, MoCA score 6 months after stroke Computerised global cognitive score at admission and 6 months post-stroke, GDS score at admission and 6 months posts-stoke. Multivariate predictors include MoCA at admission, age greater or equal to 75 and admission GDS score greater than or equal to 6 Depressive symptoms in poststroke/TIA patients are associated with MCI or dementia and functional deterioration at 2-year follow-up. This association occurs immediately after stroke/TIA and becomes more significant 6 months after the initial stroke. Follow-upsignificant improvement in all three mean scores: TOTAL: 83.14 (SD 12.2) EF 14.6 (SD 4.9) EX 5.8 (SD 2.5) Depression influenced the performance on executive function tests as well as the overall CAMCOG-R score.
(Cognitive impairment according to RBANS Total Index Score was defined as a score <= 77.5 points, equal to 1.5 SD below mean which is recommended cut-off score for MCI. MMSE score at baseline (median (IQR)): n=104. MMSE=25 (7) RBANs index score Of the n=104, 61 (59%) were classified as cognitively impaired at baseline, compared to 52 (50%) at follow up. In total, 45 were classed as cog. Impaired at both occasions (persistent cases), 7 of the non-impaired at baseline switched to impaired at follow up, 16 were classed as cognitively impaired at baseline but switched to non-impaired at follow up (recovery cases) A significant dose-dependent effect of the APOE-genotype in relation to overall post-stroke cognitive functioning was found at baseline and follow-up, but not pre-stroke. The e4 carriers showed a significant decline in tests related to verbal learning and memory compared to the non-carriers.
Four factors at baseline were independently associated with cognitive impairment at 13 months after acute stroke: Previous stroke, higher IQCODE score (indicating poorer pre-stroke cognitive functioning), higher NIHSS score (indicating more severe strokes) and the presence of one or two e4-alleles. NOT REPORTED NOT REPORTED Participants with a history of stroke (model 0: adjusted for 3MS) had an annualised loss of 1.6 (95% confidence interval -2.1, -1.1) points per year more than those without previous stroke.
Participants with baseline stroke (model 1: adjusted for prior 3MS, age, sex, race, education, income, smoking, hypertension, antihypertensive and antidepressant medication use, prior diabetes and prior coronary heart disease) had an average 3MS decline of 1.2 (95% confidence interval [CI]: 0.7-1.7) points per year more than those without one.
Results demonstrate that the rate of cognitive decline after ischemic stroke is more than double that of individuals without one. In addition, a recent left hemisphere stroke causes decline 10 times as great as that experienced by persons without one and 60% more rapid than that of persons with a recent stroke in the right hemisphere. Rowan 2007 11 Total group CAMCOG 86.6 (7.9) Executive function 14.7