White matter hyperintensities volume and cognition: A meta-analysis

Guo, Wenjuan

doi:10.3389/fnagi.2022.949763

Cited by 27 publications

(12 citation statements)

References 40 publications

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“…A multivariate analysis incorporating WMH volume, WM volume, age, and education level identified both WMH volume and WM volume as independent risk factors for cognitive impairment. A previous meta-analysis demonstrated that WMH volume was associated with the risk of cognitive impairment and it supported our findings (Guo and Shi, 2022). A study on subclinical cerebral small vessel disease and processing speed in non-dementia patients (Hotz et al, 2021) revealed a correlation between WMH volume, normal WM volume and processing speed, also demonstrating that education level was a protective factor for WM volume and normal WM volume.…”

Section: Discussionsupporting

confidence: 90%

Value of white matter hyperintensity volume and total white matter volume for evaluating cognitive impairment in patients with cerebral small-vessel disease

Zhang

Yang

et al. 2023

Front. Aging Neurosci.

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BackgroundWhite matter hyperintensities (WMH) are a key imaging feature of cerebral small-vessel disease (CSVD). However, there is a lack of standardized methods for determining WMH volume, and the value of total white matter (WM) volume in the assessment of cognitive impairment in patients with CSVD remains unknown.ObjectiveWe aimed to explore the correlations of WMH volume and WM volume with cognitive dysfunction and its components in patients with CSVD. We also aimed to compare the value of the Fazekas score, WMH volume, and ratio of WMH volume to total WM volume in the assessment of cognitive dysfunction.MethodsThe study included 99 patients with CSVD. Patients were categorized into following groups based on MoCA scores: patients with mild cognitive impairment and those without. Brain magnetic resonance images were processed to investigate differences in WMH and WM volumes between the groups. Logistic regression analysis was used to determine whether these two factors were independent risk factors for cognitive dysfunction. Correlation analysis was used to examine the relationships of WMH and WM volume with different types of cognitive impairment. Receiver operating characteristic curves were used to compare the effectiveness of the WMH score, WMH volume, and WMH to WM ratio for evaluating cognitive dysfunction.ResultsThere were significant differences in age, education level, WMH volume, and WM volume between the groups (P < 0.05). After adjusting for age and education, the multivariate logistic analysis indicated that both WMH volume and WM volume were independent risk factors for cognitive dysfunction. Correlation analysis indicated that WMH volume was mainly related to cognition involving the visual space and delayed recall. WM volume was not strongly associated with different types of cognitive dysfunction. The WMH to WM ratio was the strongest predictor, with an area under the curve value of 0.800 and a 95% confidence interval of 0.710–0.891.ConclusionIncreases in WMH volume may aggravate cognitive dysfunction in patients with CSVD, and a higher WM volume may reduce the effect of WMH volume on cognitive function to a certain extent. The ratio of WMH to total WM volume may reduce the impact of brain atrophy, allowing for more accurate evaluation of cognitive dysfunction in older adults with CSVD.

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Section: Discussionsupporting

confidence: 90%

Value of white matter hyperintensity volume and total white matter volume for evaluating cognitive impairment in patients with cerebral small-vessel disease

Zhang

Yang

et al. 2023

Front. Aging Neurosci.

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“…Overall, of all vascular phenotypes considered, WMH appeared to show the most robust associations with dementia risk, including AD, AD-meta, and all-cause dementia, adding evidence of causal associations to findings from observational studies and highlighting WMH as a key pathway to target for dementia prevention (eFigure 5 in Supplement 2). This finding reinforces earlier observations of a putative causal association of WMH with AD-meta, expanding it to a larger AD-meta GWAS and to clinically diagnosed AD .…”

Section: Discussionmentioning

confidence: 74%

Genetic Complexities of Cerebral Small Vessel Disease, Blood Pressure, and Dementia

Sargurupremraj,

Soumaré,

Bis

et al. 2024

JAMA Netw Open

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ImportanceVascular disease is a treatable contributor to dementia risk, but the role of specific markers remains unclear, making prevention strategies uncertain.ObjectiveTo investigate the causal association between white matter hyperintensity (WMH) burden, clinical stroke, blood pressure (BP), and dementia risk, while accounting for potential epidemiologic biases.Design, Setting, and ParticipantsThis study first examined the association of genetically determined WMH burden, stroke, and BP levels with Alzheimer disease (AD) in a 2-sample mendelian randomization (2SMR) framework. Second, using population-based studies (1979-2018) with prospective dementia surveillance, the genetic association of WMH, stroke, and BP with incident all-cause dementia was examined. Data analysis was performed from July 26, 2020, through July 24, 2022.ExposuresGenetically determined WMH burden and BP levels, as well as genetic liability to stroke derived from genome-wide association studies (GWASs) in European ancestry populations.Main Outcomes and MeasuresThe association of genetic instruments for WMH, stroke, and BP with dementia was studied using GWASs of AD (defined clinically and additionally meta-analyzed including both clinically diagnosed AD and AD defined based on parental history [AD-meta]) for 2SMR and incident all-cause dementia for longitudinal analyses.ResultsIn 2SMR (summary statistics–based) analyses using AD GWASs with up to 75 024 AD cases (mean [SD] age at AD onset, 75.5 [4.4] years; 56.9% women), larger WMH burden showed evidence for a causal association with increased risk of AD (odds ratio [OR], 1.43; 95% CI, 1.10-1.86; P = .007, per unit increase in WMH risk alleles) and AD-meta (OR, 1.19; 95% CI, 1.06-1.34; P = .008), after accounting for pulse pressure for the former. Blood pressure traits showed evidence for a protective association with AD, with evidence for confounding by shared genetic instruments. In the longitudinal (individual-level data) analyses involving 10 699 incident all-cause dementia cases (mean [SD] age at dementia diagnosis, 74.4 [9.1] years; 55.4% women), no significant association was observed between larger WMH burden and incident all-cause dementia (hazard ratio [HR], 1.02; 95% CI, 1.00-1.04; P = .07). Although all exposures were associated with mortality, with the strongest association observed for systolic BP (HR, 1.04; 95% CI, 1.03-1.06; P = 1.9 × 10−14), there was no evidence for selective survival bias during follow-up using illness-death models. In secondary analyses using polygenic scores, the association of genetic liability to stroke, but not genetically determined WMH, with dementia outcomes was attenuated after adjusting for interim stroke.ConclusionsThese findings suggest that WMH is a primary vascular factor associated with dementia risk, emphasizing its significance in preventive strategies for dementia. Future studies are warranted to examine whether this finding can be generalized to non-European populations.

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Section: Discussionmentioning

confidence: 99%

“…Regarding the impact of white matter damage, there is a robust body of evidence to suggest that white matter damage results in cognitive impairment, although to our knowledge, this has not been comprehensively studied in dedicated large vessel occlusion stroke data sets yet. As an example, white matter damage is closely associated with cognitive impairment in patients with cerebrovascular small vessel disease 22 and traumatic brain injury. 23 With regard to AIS specifically, Cha et al showed that unilateral spatial neglect seems to results from damage to white matter tracts such as the superior longitudinal fasciculus and forceps minor, 24 and Schevenels et al found that disruption of white matter tracts in patients with aphasic stroke results is negatively associated with language recovery in the first months after stroke.…”

Section: Discussionmentioning

confidence: 99%

Influence of Infarct Morphology and Patterns on Cognitive Outcomes After Endovascular Thrombectomy

Ospel,

Rinkel,

Ganesh

et al. 2024

Stroke

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BACKGROUND: To assess the association of qualitative and quantitative infarct characteristics and 3 cognitive outcome tests, namely the Montreal Cognitive Assessment (MOCA) for mild cognitive impairment, the Boston Naming Test for visual confrontation naming, and the Sunnybrook Neglect Assessment Procedure for neglect, in large vessel occlusion stroke. METHODS: Secondary observational cohort study using data from the randomized-controlled ESCAPE-NA1 trial (Safety and Efficacy of Nerinetide in Subjects Undergoing Endovascular Thrombectomy for Stroke), in which patients with large vessel occlusion undergoing endovascular treatment were randomized to receive either intravenous Nerinetide or placebo. MOCA, Sunnybrook Neglect Assessment Procedure, and 15-item Boston Naming Test were obtained at 90 days. Total infarct volume, grey matter, and white matter infarct volumes were manually measured on 24-hour follow-up imaging. Infarcts were also visually classified as either involving the grey matter only or both the grey and white matter and scattered versus territorial. Associations of infarct variables and cognitive outcomes were analyzed using multivariable ordinal or binary logistic regression models. RESULTS: Of 1105 patients enrolled in ESCAPE-NA1, 1026 patients with visible infarcts on 24-hour follow-up imaging were included. MOCA and Sunnybrook Neglect Assessment Procedure were available for 706 (68.8%) patients and the 15-item Boston Naming Test was available for 682 (66.5%) patients. Total infarct volume was associated with worse MOCA scores (adjusted common odds ratio per 10 mL increase, 1.05 [95% CI, 1.04–1.06]). After adjusting for baseline variables and total infarct volume, mixed grey and white matter involvement (versus grey matter-only adjusted common odds ratio, 1.92 [95% CI, 1.37–2.69]), white matter infarct volume (adjusted common odds ratio per 10 mL increase 1.36 [95% CI, 1.18–1.58]) and territorial (versus scattered) infarct pattern (adjusted common odds ratio, 1.65 [95% CI, 1.15–2.38]) were associated with worse MOCA scores. Results for Sunnybrook Neglect Assessment Procedure and 15-item Boston Naming Test were similar, except for the territorial infarct pattern, which did not reach statistical significance in multivariable analysis. CONCLUSIONS: Besides total infarct volume, infarcts that involve the white matter and that show a territorial distribution were associated with worse cognitive outcomes, even after adjusting for total infarct volume.

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White matter hyperintensities volume and cognition: A meta-analysis

Cited by 27 publications

References 40 publications

Value of white matter hyperintensity volume and total white matter volume for evaluating cognitive impairment in patients with cerebral small-vessel disease

Value of white matter hyperintensity volume and total white matter volume for evaluating cognitive impairment in patients with cerebral small-vessel disease

Genetic Complexities of Cerebral Small Vessel Disease, Blood Pressure, and Dementia

Influence of Infarct Morphology and Patterns on Cognitive Outcomes After Endovascular Thrombectomy

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