Small white matter lesion detection in cerebral small vessel disease

Abstract Cerebral small vessel disease is a common disease in the older population and is recognized as a major risk factor for cognitive decline and stroke. Small vessel disease is considered a global brain disease impacting the integrity of neuronal networks resulting in disturbances of structural and functional connectivity. A core feature of cerebral small vessel disease commonly present on neuroimaging is white matter hyperintensities. We studied high-resolution resting-state EEG, leveraging source reconstruction methods, in 35 participants with varying degree of white matter hyperintensities without clinically evident cognitive impairment in an observational study. In patients with increasing white matter lesion load, global theta power was increased independently of age. Whole-brain functional connectivity revealed a disrupted network confined to the alpha band in participants with higher white matter hyperintensities lesion load. The decrease of functional connectivity was evident in long-range connections, mostly originating or terminating in the frontal lobe. Cognitive testing revealed no global cognitive impairment; however, some participants revealed deficits of executive functions that were related to larger white matter hyperintensities lesion load. In summary, participants without clinical signs of mild cognitive impairment or dementia showed oscillatory changes that were significantly related to white matter lesion load. Hence, oscillatory neuronal network changes due to white matter lesions might act as biomarker prior to clinically relevant behavioural impairment.

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White matter lesion progression: A surrogate endpoint for trials in cerebral small-vessel disease

Neurology ◽

10.1212/01.wnl.0000132635.75819.e5 ◽

2004 ◽

Vol 63 (1) ◽

pp. 139-144 ◽

Cited By ~ 117

Author(s):

R. Schmidt ◽

Ph. Scheltens ◽

T. Erkinjuntti ◽

L. Pantoni ◽

H. S. Markus ◽

...

Keyword(s):

White Matter ◽

Small Vessel Disease ◽

White Matter Lesion ◽

Surrogate Endpoint ◽

Cerebral Small Vessel Disease ◽

Small Vessel ◽

Vessel Disease

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Higher Cerebral Small Vessel Disease Burden in Patients with White Matter Recent Small Subcortical Infarcts

Journal of Stroke and Cerebrovascular Diseases ◽

10.1016/j.jstrokecerebrovasdis.2021.105824 ◽

2021 ◽

Vol 30 (7) ◽

pp. 105824

Author(s):

Salvatore Rudilosso ◽

Luis Mena ◽

Diana Esteller ◽

Marta Olivera ◽

Juan José Mengual ◽

...

Keyword(s):

White Matter ◽

Disease Burden ◽

Small Vessel Disease ◽

Cerebral Small Vessel Disease ◽

Small Vessel ◽

Vessel Disease

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Cognitive heterogeneity among community-dwelling older adults with Cerebral Small Vessel Disease

10.31234/osf.io/692bf ◽

2018 ◽

Author(s):

Ayan Dey ◽

Vessela Stamenova ◽

Agnes Bacopulos ◽

Nivethika Jeyakumar ◽

Gary R. Turner ◽

...

Keyword(s):

White Matter ◽

Subjective Experience ◽

Small Vessel Disease ◽

Neuropsychological Testing ◽

Cerebral Small Vessel Disease ◽

Community Dwelling ◽

Small Vessel ◽

Vessel Disease ◽

Age Related ◽

Subjective Complaints

Some degree of ischemic injury to white matter tracts occurs naturally with age and is visible on magnetic resonance imaging as focal or confluent white matter hyperintensities (WMHs). Its relationship to cognition, however, remains unclear. To explore this, community-dwelling adults between the ages 55-80 years old completed structural imaging, neuropsychological testing, and questionnaires to provide objective measures and subjective experience of executive functioning. Volumetric lesion burden derived from structural MRI identified those with significant WMH burden (~10 cubic cm). Half of those recruited met this criterion and were designated as the cerebral small vessel disease (CSVD) group. Subjective complaints but not objective test scores differentiated adults with and without CSVD. Hierarchical clustering revealed two CSVD subgroups that differentiated those with impaired versus preserved executive function relative to controls. Overall these results provide some explanation for behavioural heterogeneity often observed in studies of age-related white matter changes. They also support the use of questionnaires to assess subjective complaints that may be able to detect subtle effects of pathology not evident on standardized cognitive scores.

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Abstract P369: Cerebral Small Vessel Disease and Enlarged Cardiac Ventricles

Stroke ◽

10.1161/str.52.suppl_1.p369 ◽

2021 ◽

Vol 52 (Suppl_1) ◽

Author(s):

Kayla Navarro ◽

Ka-ho Wong ◽

Majd M Ibrahim ◽

Adam H De Havenon ◽

Eric Goldstein

Keyword(s):

White Matter ◽

Ejection Fraction ◽

Right Ventricular ◽

Small Vessel Disease ◽

Cerebral Small Vessel Disease ◽

Small Vessel ◽

Right Atrial ◽

Ventricular Ejection Fraction ◽

Vessel Disease ◽

Atrial Area

Introduction: White matter hyperintensities (WMH) are a radiographic marker for cerebral small vessel disease (CSVD). Conditions altering cerebral venous outflow such as elevated central venous pressure and right atrial pressure in individuals with cardiac valvular disease have been implicated in the development of WMH. Hypothesis: We hypothesize that increased right-heart chamber size in individuals without significant cardiac valvular disease is associated with worse WMH. Methods: A retrospective chart review of adults with a brain MRI and a 2-dimensional transthoracic echocardiogram (TTE) was performed. Worst burden of WMH by way of Fazekas score, either periventricular or deep white matter, served as the primary outcome. Statistical analysis was performed using a multivariate ordinal logistic regression model. Results: A total of 132 individuals were included. Right atrial area (OR 0.93, 95% CI 0.87 to 1.00, p = 0.0041), right ventricular internal diameter (OR 0.48, 95%CI 0.27 to 0.83, p = 0.008) and left atrial area (OR 0.93, 95%CI 0.88 to 0.98, p = 0.007) was identified as being significant. Cardiac functional markers were not significant, including tricuspid annular plane systolic excursion (OR 0.99, 95%CI 0.93 to 1.05, p = 0.670), right ventricular ejection fraction (OR 0.99, 95%CI 0.96 to 1.02, p = 0.670) and left ventricular ejection fraction (OR 0.99, 95%CI 0.96 to 1.02, p = 0.567). Analysis of isolated DWM or PVWM Fazekas scores did not find significant predictors in relation to cardiac structure or function. Conclusions: Through non-invasive cardiac imaging, we identified that cardiac structural abnormalities as opposed to functional abnormalities were associated with worse WMH. Mechanistically this may result from altered intracerebral arteriovenous coupling or a shared pathophysiologic pathway between WMH and coronary microvascular disease.

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Abstract TMP119: High Homocysteine Level is not Associated With White Matter Changes, Dementia nor Mortality After Ischemic Stroke

Stroke ◽

10.1161/str.47.suppl_1.tmp119 ◽

2016 ◽

Vol 47 (suppl_1) ◽

Author(s):

Susanna Melkas ◽

Sami Curtze ◽

Gerli Sibolt ◽

Niku K Oksala ◽

Jukka Putaala ◽

...

Keyword(s):

Ischemic Stroke ◽

White Matter ◽

Homocysteine Level ◽

Small Vessel Disease ◽

Cerebral Small Vessel Disease ◽

Small Vessel ◽

Cross Sectional ◽

White Matter Changes ◽

Vessel Disease

Background: Association between high homocysteine level and cerebral small-vessel disease has been implicated in cross-sectional studies, but results from longitudinal studies have been less clear. The aim of this study was to investigate whether homocysteine level at 3-months poststroke relates to the occurrence of white matter changes (WMC), the surrogate of cerebral small-vessel disease. We also investigated whether it relates to the prognosis after ischemic stroke regarding the risk of dementia at 3-months and mortality in long-term follow-up. Methods: A total of 321 consecutive acute ischemic stroke patients aged 55 to 85 were included in the study and followed up to 12 years. Plasma homocysteine level and occurrence of WMC in MRI were measured 3 months poststroke and dementia according to DSM-III was evaluated at the same time. Findings: The median homocysteine level was 13.50 μmol/l (interquartile range [IQR] 10.60-18.50 μmol/l). Total of 81 patients (25.2%) had homocysteine level above 18.50 μmol/l. In logistic regression analysis, homocysteine level above 18.50 μmol/l was not associated with severe WMC nor with dementia at 3 months poststroke. In Kaplan-Meier analysis, homocysteine level above 18.50 μmol/l was not associated with survival in 12-year follow-up. For further analysis, the group was divided in quartiles according to homocysteine level. The quartiles did not differ in occurrence of severe WMC at baseline, in the risk of dementia at 3 months, nor in the risk of mortality in 12-year follow-up. Interpretation: In our poststroke cohort homocysteine level is not associated with WMC. Further, it does not relate to impaired prognosis manifested as dementia at 3 months or mortality in 12-year follow-up.

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Abstract TP512: White Matter Lesion Volume Change and Antiplatelet Treatment in Small Vessel Disease; Quantitative Analysis From Picasso Study

Stroke ◽

10.1161/str.50.suppl_1.tp512 ◽

2019 ◽

Vol 50 (Suppl_1) ◽

Author(s):

Bum Joon Kim ◽

Sun U Kwon ◽

Yong-Hwan Kim ◽

Dong-Wha Kang

Keyword(s):

Quantitative Analysis ◽

White Matter ◽

Volume Change ◽

Small Vessel Disease ◽

White Matter Lesion ◽

Small Vessel ◽

Lesion Volume ◽

Antiplatelet Treatment ◽

Vessel Disease

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A Systematic Review of WNT Signaling in Endothelial Cell Oligodendrocyte Interactions: Potential Relevance to Cerebral Small Vessel Disease

Cells ◽

10.3390/cells9061545 ◽

2020 ◽

Vol 9 (6) ◽

pp. 1545

Author(s):

Narek Manukjan ◽

Zubair Ahmed ◽

Daniel Fulton ◽

W. Matthijs Blankesteijn ◽

Sébastien Foulquier

Keyword(s):

White Matter ◽

Small Vessel Disease ◽

Clinical Manifestations ◽

Cell Types ◽

Cerebral Small Vessel Disease ◽

White Matter Injury ◽

Small Vessel ◽

Limited Attention ◽

Vessel Disease

Key pathological features of cerebral small vessel disease (cSVD) include impairment of the blood brain barrier (BBB) and the progression of white matter lesions (WMLs) amongst other structural lesions, leading to the clinical manifestations of cSVD. The function of endothelial cells (ECs) is of major importance to maintain a proper BBB. ECs interact with several cell types to provide structural and functional support to the brain. Oligodendrocytes (OLs) myelinate axons in the central nervous system and are crucial in sustaining the integrity of white matter. The interplay between ECs and OLs and their precursor cells (OPCs) has received limited attention yet seems of relevance for the study of BBB dysfunction and white matter injury in cSVD. Emerging evidence shows a crosstalk between ECs and OPCs/OLs, mediated by signaling through the Wingless and Int-1 (WNT)/β-catenin pathway. As the latter is involved in EC function (e.g., angiogenesis) and oligodendrogenesis, we reviewed the role of WNT/β-catenin signaling for both cell types and performed a systematic search to identify studies describing a WNT-mediated interplay between ECs and OPCs/OLs. Dysregulation of this interaction may limit remyelination of WMLs and render the BBB leaky, thereby initiating a vicious neuroinflammatory cycle. A better understanding of the role of this signaling pathway in EC–OL crosstalk is essential in understanding cSVD development.

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