scholarly journals Correlations in post‐mortem imaging‐histopathology studies of sporadic human cerebral small vessel disease: a systematic review

2021 ◽  
Author(s):  
Catherine A Humphreys ◽  
Colin Smith ◽  
Joanna M Wardlaw
Keyword(s):  
Systematic Review ◽  
Small Vessel Disease ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Post Mortem ◽  
Vessel Disease

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 Inflammation and cerebral small vessel disease: A systematic review

2019 ◽  
Vol 53 ◽  
pp. 100916 ◽  
Author(s):  
Audrey Low ◽  
Elijah Mak ◽  
James B. Rowe ◽  
Hugh S. Markus ◽  
John T. O’Brien
Keyword(s):  
Systematic Review ◽  
Small Vessel Disease ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Vessel Disease

scholarly journals Cognitive impairment in sporadic cerebral small vessel disease: A systematic review and meta‐analysis

2020 ◽  
Author(s):  
Olivia K. L. Hamilton ◽  
Ellen V. Backhouse ◽  
Esther Janssen ◽  
Angela C. C. Jochems ◽  
Caragh Maher ◽  
...  
Keyword(s):  
Systematic Review ◽  
Cognitive Impairment ◽  
Small Vessel Disease ◽  
Meta Analysis ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Vessel Disease

scholarly journals Do in vivo Experimental Models Reflect Human Cerebral Small Vessel Disease? a Systematic Review

2008 ◽  
Vol 28 (12) ◽  
pp. 1877-1891 ◽  
Author(s):  
Atticus H Hainsworth ◽  
Hugh S Markus
Keyword(s):  
Systematic Review ◽  
White Matter ◽  
Small Vessel Disease ◽  
Experimental Models ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Genetic Mutations ◽  
Ischaemic Injury ◽  
Vessel Disease ◽  
Diffuse White Matter

Cerebral small vessel disease (SVD) is a major cause of stroke and dementia. Pathologically, three lesions are seen: small vessel arteriopathy, lacunar infarction, and diffuse white matter injury (leukoaraiosis). Appropriate experimental models would aid in understanding these pathologic states and also in preclinical testing of therapies. The objective was to perform a systematic review of animal models of SVD and determine whether these resemble four key clinicopathologic features: (1) small, discrete infarcts; (2) small vessel arteriopathy; (3) diffuse white matter damage; (4) cognitive impairment. Fifteen different models were included, under four categories: (1) embolic injuries (injected blood clot, photochemical, detergent-evoked); (2) hypoperfusion/ischaemic injury (bilateral common carotid occlusion/stenosis, striatal endothelin-1 injection, striatal mitotoxin 3-NPA); (3) hypertension-based injuries (surgical narrowing of the aorta, or genetic mutations, usually in the renin-angiotensin system); (4) blood vessel damage (injected proteases, endothelium-targeting viral infection, or genetic mutations affecting vessel walls). Chronic hypertensive models resembled most key features of SVD, and shared the major risk factors of hypertension and age with human SVD. The most-used model was the stroke-prone spontaneously hypertensive rat (SHR-SP). No model described all features of the human disease. The optimal choice of model depends on the aspect of pathophysiology being studied.

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