scholarly journals Linking cortical atrophy to white matter hyperintensities of presumed vascular origin

2020 ◽  
pp. 0271678X2097417
Author(s):  
Carola Mayer ◽  
Benedikt M Frey ◽  
Eckhard Schlemm ◽  
Marvin Petersen ◽  
Kristin Engelke ◽  
...  

We examined the relationship between white matter hyperintensities (WMH) and cortical neurodegeneration in cerebral small vessel disease (CSVD) by investigating whether cortical thickness is a remote effect of WMH through structural fiber tract connectivity in a population at increased risk of CSVD. We measured cortical thickness on T1-weighted images and segmented WMH on FLAIR images in 930 participants of a population-based cohort study at baseline. DWI-derived whole-brain probabilistic tractography was used to define WMH connectivity to cortical regions. Linear mixed-effects models were applied to analyze the relationship between cortical thickness and connectivity to WMH. Factors associated with cortical thickness (age, sex, hemisphere, region, individual differences in cortical thickness) were added as covariates. Median age was 64 [IQR 46–76] years. Visual inspection of surface maps revealed distinct connectivity patterns of cortical regions to WMH. WMH connectivity to the cortex was associated with reduced cortical thickness ( p = 0.009) after controlling for covariates. This association was found for periventricular WMH ( p = 0.001) only. Our results indicate an association between WMH and cortical thickness via connecting fiber tracts. The results imply a mechanism of secondary neurodegeneration in cortical regions distant, yet connected to subcortical vascular lesions, which appears to be driven by periventricular WMH.

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Daiki Takano ◽  
Takashi Yamazaki ◽  
Tetsuya Maeda ◽  
Yuichi Satoh ◽  
Yasuko Ikeda ◽  
...  

[Introduction] White matter hyperintensities (WMH) are considered manifestation of arteriosclerotic small vessel disease and WMH burden increases risk of ischemic stroke and cognitive decline. There are only a few evidences concerning the relationship between polyunsaturated fatty acids (PUFA) and WMH. The present study was designed to elucidate the association between WMH and PUFA profile including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and arachidonic acid (AA) in patients with Alzheimer’s disease (AD). [Methods] The present study was based on 119 patients who were diagnosed as having a probable AD according to the NINCDS-ADRDA criteria. Their mean age was 78.3 years old. All subjects underwent neuropsychological evaluation including mini mental state exam (MMSE) and 1.5-Tesla MRI. Fasting blood samples were also collected for the PUFA measurements. We measured the ratio of serum EPA, DHA and AA concentration to the total PUFA concentration. The WMH were evaluated on T2-weight images and classified into periventricular hyperintensity (PVH) and deep white matter hyperintensity (DWMH). The severity of WMH was graded 5 categories. We investigated the relationship between WMH and PUFA profiles. [Results] The EPA ratio correlated negatively with both PVH (rs=-0.2036, p=0.0264) and DWMH grade (rs=-0.3155, p=0.0005). It remained still significant after adjustment for age, sex, statins use, antithrombotics use, mean blood pressure and presence of hypertension (standardized partial regression coefficient(β)=-0.2516, p=0.0122 for PVH, β=-0.3598, p=0.0001 for DWMH). Neither DHA nor AA ratio correlated with DWMH or PVH grade. The EPA ratio but not DHA or AA ratio correlated positively with total MMSE score (rs=0.2310, p=0.0115). [Conclusions] Our data revealed that the serum EPA was protective against WMH as well as cognitive decline in AD patients. Pathophysiology underlying WMH is complex and the possible mechanisms involved in the pathogenesis of WMH encompass incomplete brain ischemia, increased permeability of blood-brain barrier, and inflammation responses. The relationship between serum EPA and WMH can be partly explained by those anti-ischemic and anti-arteriosclerotic effects of EPA.


2021 ◽  
Author(s):  
Miracle Ozzoude ◽  
Brenda Varriano ◽  
Derek Beaton ◽  
Joel Ramirez ◽  
Melissa F Holmes ◽  
...  

Introduction: Change in empathy is an increasingly recognised symptom of neurodegenerative diseases and contributes to caregiver burden and patient distress. Empathy impairment has been associated with brain atrophy but its relationship to white matter hyperintensities (WMH) is unknown. We aimed to investigate the relationships amongst WMH, brain atrophy, and empathy deficits in neurodegenerative and cerebrovascular diseases. Methods: 513 participants with Alzheimers Disease/Mild Cognitive Impairment, Amyotrophic Lateral Sclerosis, Frontotemporal Dementia (FTD), Parkinsons Disease, or Cerebrovascular Disease (CVD) were included. Empathy was assessed using the Interpersonal Reactivity Index. WMH were measured using a semi-automatic segmentation and FreeSurfer was used to measure cortical thickness. Results: A heterogeneous pattern of cortical thinning was found between groups, with FTD showing thinning in frontotemporal regions and CVD in left superior parietal, left insula, and left postcentral. Results from both univariate and multivariate analyses revealed that several variables were associated with empathy, particularly cortical thickness in the fronto-insulo-temporal and cingulate regions, sex(female), global cognition, and right parietal and occipital WMH. Conclusions: Our results suggest that cortical atrophy and WMH may be associated with empathy deficits in neurodegenerative and cerebrovascular diseases. Future work should consider investigating the longitudinal effects of WMH and atrophy on empathy deficits in neurodegenerative and cerebrovascular diseases.


Author(s):  
Janine Gronewold ◽  
Martha Jokisch ◽  
Sara Schramm ◽  
Christiane Jockwitz ◽  
Tatiana Miller ◽  
...  

White matter hyperintensities (WMHs) of presumed vascular origin are a frequent finding in cerebral magnetic resonance imaging of older people. They are attributed to small vessel disease and involved in the pathogenesis of cognitive decline. Since vascular risk factors, especially arterial hypertension, predispose to small vessel disease, we analyzed the association of systolic blood pressure (SBP), diastolic blood pressure (DBP), and antihypertensive medications with WMH volume in 560 participants of the 1000BRAINS study, drawn from the population-based Heinz Nixdorf Recall study (65.2±7.5 years; 51.4% men). Further, we analyzed treatment efficacy using a classification of 6 BP treatment groups defined by antihypertensive medication and level of BP: (1) untreated BP <120/<80 mm Hg, (2) untreated SBP 120 to 139 or DBP 80 to 89 mm Hg, (3) untreated BP ≥140 or ≥90 mm Hg, (4) treated BP <120/<80 mm Hg, (5) treated SBP 120 to 139 or DBP 80 to 89 mm Hg, and (6) treated BP ≥140 or ≥90 mm Hg. Median WMH volume (Q1–Q3) was 4.6 (3.0–7.8) cm 3 ; mean±SD of SBP and DBP was 128.6±17.4 and 76.1±9.8 mm Hg. In multivariable linear regression models, continuous SBP (β=0.63 cm 3 per 10 mm Hg [95% CI, 0.32–0.94]), DBP (0.64 cm 3 per 5 mmHg [95% CI, 0.37–0.91]), and antihypertensive treatment (1.23 cm 3 [95% CI, 0.14–2.23]) were significantly associated with WMH volume. Regarding treatment efficacy, only participants with hypertension despite treatment (treated BP ≥140 or ≥90 mm Hg) had significantly increased WMH volume (4.24 cm 3 [2.36–6.13]) compared with normotension without treatment (untreated BP <120/<80 mm Hg). Our results suggest that WMHs represent a marker of advanced hypertension pathology. Hence, early treatment should prevent WMHs.


2020 ◽  
Vol 75 (8) ◽  
pp. 1545-1550
Author(s):  
Timothy P Siejka ◽  
Velandai K Srikanth ◽  
Ruth E Hubbard ◽  
Chris Moran ◽  
Richard Beare ◽  
...  

Abstract Background The contribution of cerebral small vessel disease (cSVD) to the pathogenesis of frailty remains uncertain. We aimed to examine the associations between cSVD with progression of frailty in a population-based study of older people. Methods People aged between 60 and 85 years were randomly selected form the electoral roll to participate in the Tasmanian Study of Cognition and Gait. Participants underwent self-reported questionnaires, objective gait, cognitive and sensorimotor testing over three phases ranging between 2005 and 2012. These data were used to calculate a 41-item frailty index (FI) at three time points. Baseline brain magnetic resonance imaging was performed on all participants to measure cSVD. Generalized mixed models were used to examine associations between baseline cSVD and progression of frailty, adjusted for confounders of age, sex, level of education, and total intracranial volume. Results At baseline (n = 388) mean age was 72 years (SD = 7.0), 44% were female, and the median FI score was 0.20 (interquartile range [IQR] 0.12, 0.27). In fully adjusted models higher burden of baseline white matter hyperintensity (WMH) was associated with frailty progression over 4.4 years (β = 0.03, 95% CI: 0.01, 0.05; p = .004) independent of other SVD markers. Neither baseline infarcts (p = .23), nor microbleeds at baseline (p = .65) were associated with progression of frailty. Conclusions We provide evidence for an association between baseline WMHs and progression of frailty. Our findings add to a growing body of literature suggesting WMH is a marker for frailty.


Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Sang-mi Noh ◽  
Jong S. Kim

Background: Gastrointestinal (GI) bleeding is a major complication of aniplatelets in patients with stroke. Although underlying gastrointestinal disease is an important factor for increased bleeding risk, the presence of cerebral small vessel disease (SVD) may also be a factor because it may indicate systemic small vessel pathologies. We assessed the association of cerebral SVD and GI bleeding in patients who are under treatment with antiplatelets for secondary stroke prevention. Methods: We compared stroke patients who visited our clinic between May 2007 and May 2013 who developed GI bleeding while receiving antiplatelets with age and sex matched patients who did not. Control subjects were randomly selected among those who were visited out-patients clinic on the same day as the study subjects. Patients who received anticoagulants were excluded. MRIs were evaluated for the presence of white matter changes (Fazeka scale) and microbleeds. Results: During the study period, 47 patients in the bleeding group and 94 patients in the control group were enrolled. No differences were found in baseline characteristics between the two groups including stroke subtypes and the number of antiplatelets (mono vs dual therapy). The prevalence of SVD (microbleeds or white matter hyperintensities) (p = 0.004), white matter hyperintensities (p = 0.008), but not microbleeds alone (p = 0.221), were significantly higher in the bleeding group. Multivariate analysis showed that the presence of SVD was independently associated with increased GI bleeding risk (OR 3.3, 95% confidence interval 1.5-7.3). Conclusions: Our data show the presence of cerebral SVD is a marker for increased GI bleeding risk in patients receiving antiplatelets in stroke patients, perhaps related with systemic small vessel pathology in this group of patients. Physicians may have to consider this association when antiplatelets are used for the secondary prevention of stroke.


Cephalalgia ◽  
2015 ◽  
Vol 36 (2) ◽  
pp. 113-121 ◽  
Author(s):  
Lasse-Marius Honningsvåg ◽  
Knut Hagen ◽  
Asta Håberg ◽  
Lars Jacob Stovner ◽  
Mattias Linde

Background Most studies on intracranial abnormalities among headache sufferers were performed in selected clinical populations. The aim of this study was to evaluate the relationship between intracranial abnormalities and headache among middle-aged adults in the general population. Methods Participants in a large epidemiological study (the HUNT 3 study; 2006–2008) who answered a headache questionnaire and participated in a population-based imaging study of the head (HUNT MRI; 2007–2009) were included ( n = 864; age, 50–65 at enrollment). Based on the responses to the HUNT 3 questionnaire, respondents were categorized as having migraine, tension-type headache, or unclassified headache. Logistic regression was used to compare the occurrence of intracranial abnormalities between groups. Results Intracranial abnormalities were more common in headache sufferers than in headache-free individuals (29% vs. 22%, respectively; p = 0.041). Adjusted multivariate analyses revealed that those with tension-type headache had higher odds of having minor abnormalities (odds ratio, 2.13; 95% confidence interval = 1.18–3.85). This association disappeared when those with only white matter hyperintensities were removed from the analysis. Conclusions Headache sufferers had increased odds of minor intracranial abnormalities. The increased odds were primarily related to the presence of white matter hyperintensities.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 748-748
Author(s):  
C Elizabeth Shaaban ◽  
Caterina Rosano ◽  
Heather Shattuck-Heidorn ◽  
Sara Godina ◽  
Minjie Wu ◽  
...  

Abstract Women have a greater burden than men of white matter hyperintensities (WMH), a marker of cerebral small vessel disease (cSVD). Psychosocial factors including education, household income, neighborhood socioeconomic status (nSES), happiness, and depression may differ by gender and could explain women’s higher burden of WMH. In a cohort of older adults (N=250, median age=82, 58% women, 39% Black), we found that women had lower education, household income, nSES and were less happy and more depressed. Race stratified Spearman correlations showed women had greater whole brain WMH volume in white participants only (white: rho=0.23, p=0.004; Black: rho=-0.05, p=0.64). In partial Spearman correlations, education, happiness, and depression attenuated but did not fully explain the relationship when added individually or all together to the model for whites (fully adjusted rho=0.19, p=0.03). Gendered psychosocial factors may partially explain sex differences in WMH; interventions targeting these factors may reduce cSVD burden, particularly in white women.


Author(s):  
Filip Morys ◽  
Mahsa Dadar ◽  
Alain Dagher

AbstractChronic obesity is associated with several complications, including cognitive impairment and dementia. However, we have piecemeal knowledge of the mechanisms linking obesity to central nervous system damage. Adiposity leads to the metabolic syndrome, consisting of inflammation, hypertension, dyslipidemia and insulin resistance. In turn, these metabolic abnormalities cause cerebrovascular dysfunction, which may cause white and grey matter tissue loss and consequent cognitive impairment. While there have been several neuroimaging studies linking adiposity to changes in brain morphometry, a comprehensive investigation of the relationship has so far not been done. Here we use structural equation modelling applied to over 15,000 individuals from the UK Biobank to identify the causal chain that links adiposity to cognitive dysfunction. We found that body mass index and waist-to-hip ratio were positively related to higher plasma C-reactive protein, dyslipidemia, occurrence of hypertension and diabetes, all of which were in turn related to cerebrovascular disease as measured by volume of white matter hyperintensities on magnetic resonance imaging. White mater hyperintensities were associated with lower cortical thickness and volume and higher subcortical volumes, which were associated with cognitive deficits on tests of visuospatial memory, fluid intelligence, and working memory among others. In follow-up analyses we found that inflammation, hypertension and diabetes mediated 20% of the relationship between obesity and cerebrovascular disease and that cerebrovascular disease mediated a significant proportion of the relationship between obesity and cortical thickness and volume. We also showed that volume of white matter hyperintensities was related to decreased fractional anisotropy and increased mean diffusivity in the majority of white matter tracts, pointing to white matter dysconnectivity as a major cause of impaired cognition. Our results have clinical implications, supporting a role for the management of adiposity in the prevention of late-life dementia and cognitive decline.


Sign in / Sign up

Export Citation Format

Share Document