Abstract TP472: The Interplay Between Subclinical Micro- and Macro-Vascular Disease in Asymptomatic Individuals

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Ezgi Yetim ◽  
Ethem M Arsava ◽  
Kader K Oguz ◽  
Mehmet A Topcuoglu
Keyword(s):  
Basal Ganglia ◽  
Vascular Disease ◽  
Pulsatility Index ◽  
Small Vessel Disease ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Multivariate Models ◽  
Large Arteries ◽  
Vessel Disease ◽  
Carotid Distensibility

Introduction: Pathophysiological changes within large arteries, among many other factors, are considered to contribute to cerebral small vessel disease. Craniocervical sonography is a valuable tool in this regard to evaluate various physiological metrics of extra- and intra-cranial large arteries. Herein, we tried to evaluate the interplay between markers of small vessel disease, and internal carotid (ICA) and middle cerebral artery (MCA) pulsatility, carotid distensibility and intima media thickness (IMT). Methods: We prospectively evaluated a total of 278 subjects without any prior history of stroke using transcranial and cervical Doppler ultrasound, and magnetic resonance imaging. Pulsatility index was determined by Gosling’s index from bilateral MCA’s and ICA’s. We also measured carotid distensibility and IMT (by AutoIMT TM ) from both carotids and calculated their mean values. The relationship of all these sonographic metrics with imaging markers of chronic small vessel disease [lacunes, microbleeds, perivascular spaces (PVS), white matter hyperintensities (WMH)] were evaluated in multivariate models where age and cardiovascular risk factors were included as additional covariates. Results: The study population consisted of 108 males and 170 females with a mean±SD age of 64±9 years. In bivariate analyses, higher carotid IMT, higher MCA and ICA pulsatility indices, and lower carotid distensibility were significantly associated with high burden of WMH (Fazekas score of ≥2), basal ganglia PVS (PVS score ≥2) and presence of lacunes, but not with microbleeds or centrum semiovale PVS. In multivariate models, each 0.1 mm change in IMT increased the odds of severe WHM by 1.4 (95%CI 1.0-1.9), severe basal ganglia PVS by 1.4 (1.0-1.8) and lacunes by 1.6 (1.0-2.6), while no significant association remained for pulsatility index or distensibility. Conclusion: Our analyses highlight that IMT, is not only a subclinical marker of atherosclerosis, but also emerges as a factor intimately related with cerebral small vessel disease. These findings raise the possibility that IMT and cerebral small vessel disease might together reflect downstream events that culminate in vascular disease involving the large and small vessels of the brain.

scholarly journals Arterial Stiffness Is Associated With Basal Ganglia Enlarged Perivascular Spaces and Cerebral Small Vessel Disease Load

Stroke ◽  
2018 ◽  
Vol 49 (5) ◽  
pp. 1279-1281 ◽  
Author(s):  
Iolanda Riba-Llena ◽  
Joan Jiménez-Balado ◽  
Xavier Castañé ◽  
Anna Girona ◽  
Antonio López-Rueda ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Arterial Stiffness ◽  
Small Vessel Disease ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Perivascular Spaces ◽  
Vessel Disease

scholarly journals P4-078: REPRESENTATION OF BLOOD FLOW IN PERFORATING BASAL GANGLIA ARTERIES OF PATIENTS WITH CEREBRAL SMALL VESSEL DISEASE (CSVD) AT 7 TESLA MRI

2019 ◽  
Vol 15 ◽  
pp. P1304-P1304
Author(s):  
Valentina Perosa ◽  
Emrah Düzel ◽  
Tine Arts ◽  
Stefanie Schreiber ◽  
Anne Assmann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Basal Ganglia ◽  
Small Vessel Disease ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
7 Tesla ◽  
Vessel Disease ◽  
7 Tesla Mri

scholarly journals Vascular disease and multiple sclerosis: a post-mortem study exploring their relationships

Brain ◽  
2020 ◽  
Vol 143 (10) ◽  
pp. 2998-3012
Author(s):  
Ruth Geraldes ◽  
Margaret M Esiri ◽  
Rafael Perera ◽  
Sydney A Yee ◽  
Damian Jenkins ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Vascular Disease ◽  
Small Vessel Disease ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Whole Body ◽  
Post Mortem ◽  
Vessel Disease ◽  
Control Subjects ◽  
Age Range

Abstract Vascular comorbidities have a deleterious impact on multiple sclerosis clinical outcomes but it is unclear whether this is mediated by an excess of extracranial vascular disease (i.e. atherosclerosis) and/or of cerebral small vessel disease or worse multiple sclerosis pathology. To address these questions, a study using a unique post-mortem cohort wherein whole body autopsy reports and brain tissue were available for interrogation was established. Whole body autopsy reports were used to develop a global score of systemic vascular disease that included aorta and coronary artery atheroma, cardiac hypertensive disease, myocardial infarction and ischaemic stroke. The score was applied to 85 multiple sclerosis cases (46 females, age range 39 to 84 years, median 62.0 years) and 68 control cases. Post-mortem brain material from a subset of the multiple sclerosis (n = 42; age range 39–84 years, median 61.5 years) and control (n = 39) cases was selected for detailed neuropathological study. For each case, formalin-fixed paraffin-embedded tissue from the frontal and occipital white matter, basal ganglia and pons was used to obtain a global cerebral small vessel disease score that captured the presence and/or severity of arteriolosclerosis, periarteriolar space dilatation, haemosiderin leakage, microinfarcts, and microbleeds. The extent of multiple sclerosis-related pathology (focal demyelination and inflammation) was characterized in the multiple sclerosis cases. Regression models were used to investigate the influence of disease status on systemic vascular disease and cerebral small vessel disease scores and, in the multiple sclerosis group, the relationship between multiple sclerosis-related pathology and both vascular scores. We show that: (i) systemic cardiovascular burden, and specifically atherosclerosis, is lower and cerebral small vessel disease is higher in multiple sclerosis cases that die at younger ages compared with control subjects; (ii) the association between systemic vascular disease and cerebral small vessel disease is stronger in patients with multiple sclerosis compared with control subjects; and (iii) periarteriolar changes, including periarteriolar space dilatation, haemosiderin deposition and inflammation, are key features of multiple sclerosis pathology outside the classic demyelinating lesion. Our data argue against a common primary trigger for atherosclerosis and multiple sclerosis but suggest that an excess burden of cerebral small vessel disease in multiple sclerosis may explain the link between vascular comorbidity and accelerated irreversibility disability.

scholarly journals Microalbuminuria and the Combination of MRI Markers of Cerebral Small Vessel Disease

2016 ◽  
Vol 42 (1-2) ◽  
pp. 66-72 ◽  
Author(s):  
Andrea Vilar-Bergua ◽  
Iolanda Riba-Llena ◽  
Natalia Ramos ◽  
Xavier Mundet ◽  
Eugenia Espinel ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Basal Ganglia ◽  
Glomerular Filtration ◽  
Kidney Function ◽  
Filtration Rate ◽  
Small Vessel Disease ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Perivascular Spaces ◽  
Vessel Disease

Background: Kidney function has been related to the presence of individual markers of cerebral small vessel disease (CSVD), as lacunes, white matter hyperintensities (WMH) or microbleeds. We aimed at studying the relationship of kidney dysfunction with the combination of several markers of CSVD. Methods: Subjects are those included in the ISSYS cohort (Investigating Silent Strokes in hypertensives: a magnetic resonance imaging study). A scale ranging from 0 to 4 points was applied based on the presence (one point each) of lacunes, deep microbleeds, moderate to extensive basal ganglia enlarged perivascular spaces (EPVS), and periventricular or deep WMH. We determined the creatinine-based glomerular filtration rate and the urinary albumin-to-creatinine ratio (UACR) as markers of kidney function and studied their association with the scale of CSVD in univariate and ordinal logistic regression analyses. Results: Among the 975 patients included, 28.2% presented one or more CSVD markers, being the most prevalent marker (either alone or in combination) basal ganglia EPVS. The UACR was elevated at increasing the scores of the CSVD scale and remained as independent predictor of the combination of markers (common OR per natural log unit increase in UACR: 1.23, 1.07-1.41) after controlling per age, gender, cardiovascular risk, antihypertensive treatment and hypertension duration. In contrast, no associations were found between the CSVD scores and the creatinine-based estimated glomerular filtration rate. Conclusions: A significant proportion of stroke-free hypertensives present at least one imaging marker of CSVD. UACR but not creatinine-based glomerular filtration rate is associated with the combination of markers of CSVD.

Carotid atherosclerosis, dilation, and stiffness relate to cerebral small vessel disease

Neurology ◽  
2020 ◽  
Vol 94 (17) ◽  
pp. e1811-e1819
Author(s):  
Fei-Fei Zhai ◽  
Meng Yang ◽  
Yao Wei ◽  
Ming Wang ◽  
Yang Gui ◽  
...  
Keyword(s):  
White Matter ◽  
Basal Ganglia ◽  
Carotid Atherosclerosis ◽  
Small Vessel Disease ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Rational Approach ◽  
Carotid Imt ◽  
Vessel Disease ◽  
Imaging Markers

ObjectiveTo investigate the association of carotid atherosclerosis, dilation, and stiffness with imaging markers of cerebral small vessel disease (CSVD) in a community-based sample.MethodsThe study comprised 1,051 participants (age 57.5 ± 9.2 years). Carotid plaques, intima-media thickness (IMT), diastolic diameter, pulse wave velocity, and stiffness index (β) were measured by ultrasound. Imaging markers of CSVD, including lacunes, cerebral microbleeds, dilated PVS, and white matter hyperintensities (WMH) volume, were assessed.ResultsCarotid plaque was associated with the presence of lacunes (odds ratio [OR] 2.78, 95% confidence interval [CI] 1.78–4.33; p < 0.001) and larger WMH volume (natural log transformed, β ± SE, 0.32 ± 0.10; p = 0.002). The increased carotid diameter was associated with the presence of lacunes (OR 1.82, 95% CI 1.22–2.72; p = 0.003), larger WMH volume (β ± SE, 0.37 ± 0.10; p < 0.001), and PVS in the basal ganglia (OR 1.59, 95% CI 1.20–2.11; p = 0.001). Associations of carotid dilation and CSVD were independent of carotid IMT and plaque. Most parenchymal lesions were located in the basal ganglia and deep white matter. Carotid IMT and stiffness were not associated with CSVD.ConclusionsCarotid atherosclerosis and dilation are associated with imaging markers of CSVD. The noninvasive carotid assessment would seem to be a rational approach to risk stratification of CSVD.

scholarly journals Arterial branching and basal ganglia lacunes: A study in pure small vessel disease

2017 ◽  
Vol 2 (3) ◽  
pp. 264-271 ◽  
Author(s):  
Fiona C Moreton ◽  
Marco Düring ◽  
Thanh Phan ◽  
Velandai Srikanth ◽  
Richard Beare ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Pilot Study ◽  
Small Vessel Disease ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Third Order ◽  
Branching Order ◽  
Vessel Disease ◽  
Stroke Population ◽  
Weighted Magnetic Resonance Imaging

Introduction Lacunes are defined morphologically by size and location, but radiological characteristics alone may be unable to distinguish small vessel disease aetiology from alternative mechanisms. We investigated the branching order of arterial vessels associated with basal ganglia lacunes in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), in order to improve the understanding of their pathogenesis in pure cerebral small vessel disease. Patients and methods Adults with a confirmed diagnosis of CADASIL were included. A pilot study was conducted in a Scottish CADASIL cohort. The Paris–Munich CADASIL cohort was used for independent validation. Lacunes identified on T1-weighted magnetic resonance imaging scans were registered to a standard brain template. A microangiographic template of the basal ganglia vasculature was automatically overlaid onto coronal slices, and raters estimated the vessel branching order related to each lacune. Results Of 179 lacunes, 150 (84%) were associated with third-order vessels. In 14 incident lacunes, 11 (79%) were associated with third-order vessels. In the pilot study, lacune volume was significantly lower in lacunes associated with third-order vessels (0.04 ml ± 0.04 ml) compared to second-order vessels (0.48 ± 0.16 ml; p < 0.001). Discussion In this study of CADASIL patients, most lacunes were small and associated with third-order vessel disease. This suggests that these are the vessels primarily affected in cerebral small vessel disease. Microangiographic template techniques could be used to further investigate in a general stroke population whether finding large lacunes originating from higher order vessels indicates an alternative cause of stroke. Conclusion Lacunes in pure small vessel disease are associated with the smallest vessels in the basal ganglia.

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