Clinical presentations and epidemiology of vascular dementia

2017 ◽  
Vol 131 (11) ◽  
pp. 1059-1068 ◽  
Author(s):  
Eric E. Smith

Cerebrovascular and cardiovascular diseases cause vascular brain injury that can lead to vascular cognitive impairment (VCI). VCI is the second most common neuropathology of dementia and mild cognitive impairment (MCI), accounting for up to one-third of the population risk. It is frequently present along with other age-related pathologies such as Alzheimer's disease (AD). Multiple etiology dementia with both VCI and AD is the single most common cause of later life dementia. There are two main clinical syndromes of VCI: post-stroke VCI in which cognitive impairment is the immediate consequence of a recent stroke and VCI without recent stroke in which cognitive impairment is the result of covert vascular brain injury detected only on neuroimaging or neuropathology. VCI is a syndrome that can result from any cause of infarction, hemorrhage, large artery disease, cardioembolism, small vessel disease, or other cerebrovascular or cardiovascular diseases. Secondary prevention of further vascular brain injury may improve outcomes in VCI.

2021 ◽  
pp. 174749302110059
Author(s):  
Yiu Ming Bonaventure Ip ◽  
Lisa Au ◽  
Yin Yan Anne Chan ◽  
Florence Fan ◽  
Hing Lung Ip ◽  
...  

Background: Depicting the time trends of ischemic stroke subtypes may inform healthcare resource allocation on etiology-based stroke prevention and treatment. Aim: To reveal the evolving ischemic stroke subtypes from 2004 to 2018. Methods: We determined the stroke etiology of consecutive first-ever transient ischemic attack or ischemic stroke patients admitted to a regional hospital in Hong Kong from 2004 to 2018. We analyzed the age-standardized incidences and the 2-year recurrence rate of major ischemic stroke subtypes. Results: Among 6940 patients admitted from 2004 to 2018, age-standardized incidence of ischemic stroke declined from 187.0 to 127.4 per 100,000 population (p<0.001), driven by the decrease in large artery disease (43.0 to 9.67 per 100,000 population (p<0.001)) and small vessel disease (71.9 to 45.7 per 100,000 population (p<0.001)). Age-standardized incidence of cardioembolic stroke did not change significantly (p=0.2). Proportion of cardioembolic stroke increased from 20.4% in 2004-2006 to 29.3% in 2016-2018 (p<0.001). 2-year recurrence rate of intracranial atherothrombotic stroke reduced from 19.3% to 5.1% (p<0.001) with increased prescriptions of statin (p<0.001) and dual anti-platelet therapy (<0.001). In parallel with increased anticoagulation use across the study period (p<0.001), the 2-year recurrence of AF-related stroke reduced from 18.9% to 6% (p<0.001). Conclusion: Etiology-based risk factor control might have led to the diminishing stroke incidences related to atherosclerosis. To tackle the surge of AF-related strokes, arrhythmia screening, anticoagulation usage and mechanical thrombectomy service should be reinforced. Comparable preventive strategies might alleviate the enormous stroke burden in mainland China.


Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
YEONG-BAE LEE ◽  
Joo-Hwan Park ◽  
Eunja Kim ◽  
Ki-Tae Kim ◽  
Ju Kang Lee ◽  
...  

Arterial stiffness is an independent predictor of cardiovascular disease and stroke and can be evaluated by measuring pulse wave velocity(PWV) between 2 sites in the arterial tree, with a higher PWV indicating stiffer arteries. Recent studies have demonstrated that arterial stiffness is associated with intracranial large artery disease and the severity of cerebral small vessel disease. The aim of this study is to clarify whether pulse wave velocity value predict initial severity of acute ischemic stroke. We enrolled consecutive patients with acute ischemic stroke. Demographic factors, laboratory data, brain imaging, neurological exam and arterial stiffness measured by brachial ankle PWV (baPWV) were evaluated on admission in all subjects. The subtype of acute ischemic stroke was classified according to the TOAST classification. All patients were categorized into two groups based on the initial severity of stroke, indicated by modified Rankin Scale(mRS). Severe group was defined as a mRS ≥ 3 at admission. Unpaired student’s t-test or Mann-whitney U-test were used to compare maximal and meanbaPWV values between two groups. We enrolled 78 patients. According to the TOAST classification, the etiology of stroke was large artery disease (LAD) in 34 patients, small vessel disease (SVD) in 23 patients, and other subtypes in 12 patients. There were 28 patients with good outcome and 41 patients with poor outcome. The maximal and mean baPWV values were significantly increased in inpatients with high mRS score (2120.17± 527.75, 1999.21 ± 437.46) compared with those with low mRS score (1751.96 ± 363.49, 1723.14 ± 353.02)(p=0.001, p=0.007). In patients with SVD subtype, there was significant difference in maximal and mean baPWVvalues between two groups (p=0.030, p=0.047), whereas there was no significant difference in baPWV in patients with LAD subtype (p=0.141, p=0.172). The main finding of our study is that arterial stiffness indicated by baPWV is associated with the initial severity of acute ischemic stroke. Because initial stroke severity is strongly associated with functional outcome of stroke, this findings suggest that measurement of baPWV may predict long-term outcome in patients with stroke especially in those with TOAST classification confirmed as SVD.


2011 ◽  
Vol 40 (2) ◽  
pp. 175-180 ◽  
Author(s):  
C. Ramos-Estebanez ◽  
I. Moral-Arce ◽  
A. Gonzalez-Mandly ◽  
V. Dhagubatti ◽  
J. Gonzalez-Macias ◽  
...  

2018 ◽  
Vol 314 (6) ◽  
pp. H1117-H1136 ◽  
Author(s):  
Dana R. Jorgensen ◽  
C. Elizabeth Shaaban ◽  
Clayton A. Wiley ◽  
Peter J. Gianaros ◽  
Joseph Mettenburg ◽  
...  

Aging in later life engenders numerous changes to the cerebral microvasculature. Such changes can remain clinically silent but are associated with greater risk for negative health outcomes over time. Knowledge is limited about the pathogenesis, prevention, and treatment of potentially detrimental changes in the cerebral microvasculature that occur with advancing age. In this review, we summarize literature on aging of the cerebral microvasculature, and we propose a conceptual framework to fill existing research gaps and advance future work on this heterogeneous phenomenon. We propose that the major gaps in this area are attributable to an incomplete characterization of cerebrovascular pathology, the populations being studied, and the temporality of exposure to risk factors. Specifically, currently available measures of age-related cerebral microvasculature changes are indirect, primarily related to parenchymal damage rather than direct quantification of small vessel damage, limiting the understanding of cerebral small vessel disease (cSVD) itself. Moreover, studies seldom account for variability in the health-related conditions or interactions with risk factors, which are likely determinants of cSVD pathogenesis. Finally, study designs are predominantly cross-sectional and/or have relied on single time point measures, leaving no clear evidence of time trajectories of risk factors or of change in cerebral microvasculature. We argue that more resources should be invested in 1) developing methodological approaches and basic science models to better understand the pathogenic and etiological nature of age-related brain microvascular diseases and 2) implementing state-of-the-science population study designs that account for the temporal evolution of cerebral microvascular changes in diverse populations across the lifespan.


Author(s):  
Hugh Markus ◽  
Anthony Pereira ◽  
Geoffrey Cloud

This chapter on common causes of ischaemic stroke reviews the major pathologies underlying ischaemic stroke, namely large-artery disease, cardioembolism, and small-vessel disease. Large-vessel extra- and intracranial atherosclerotic cerebrovascular disease is covered. Cardioembolic aetiologies of stroke including atrial fibrillation and valvular heart disease are discussed. Small-vessel disease causing lacunar stroke and possible heterogonous pathologies underlying this subtype are covered. Dolichoectasia of arteries as a potential cause of stroke and the newer concept of embolic stroke of undetermined source are also discussed.


Author(s):  
K.D. Langdon ◽  
C. Cordova ◽  
S. Granter-Button ◽  
J. Boyd ◽  
J. Peeling ◽  
...  

Most basic science research has focused on overt stroke caused by blockage of major blood vessels. Less attention has been paid to small vessel disease giving rise to covert stroke that often leads to vascular cognitive impairment (VCI). One reason for this may be the relative lack of relevant animal models. This talk will describe a model of VCI induced in middle-aged Sprague-Dawley rats exposed to a diet high in saturated fats, salt and refined sugar (HFSS). In Experiment 1, rats fed HFSS and subjected to a small mediodorsal (MD) thalamic stroke with or without concomitant cerebral hypoperfusion experienced significant executive dysfunction. In Experiment 2, dietary influences on functional, physiological and anatomical parameters were assessed. We found significant hypertension, blockage of brain microvessels (2-photon microscopy) and white matter atrophy in HFSS diet animals. As in Experiment 1, profound, specific set-shifting executive dysfunction was noted following both small MD infarcts (0.332 mm3) and the HFSS diet. In summary, these data describe a middle-aged animal model of VCI that includes clinically-relevant metabolic disturbances and small vessel disease and as such may be helpful in developing new cognitive therapies.


2019 ◽  
Vol 28 (8) ◽  
pp. 1009-1017 ◽  
Author(s):  
Li Gong ◽  
Xiangzhu Tian ◽  
Jing Zhou ◽  
Qiong Dong ◽  
Yan Tan ◽  
...  

As a putative marker of cerebral small vessel disease, cerebral microbleeds (CMBs) have been associated with vascular cognitive impairment. Both iron accumulation and amyloid protein precursor (APP) dysregulation are recognized as pathological hallmarks underlying the progression of CMBs, but their cross-talk is not yet understood. In this study, we found a profound increase of amyloid formation with increasing FeCl3 treatment, and a distinct change in APP metabolism and expression of iron homeostasis proteins (ferritin, Fpn1, iron regulatory protein) was observed at the 300 uM concentration of FeCl3. Further results revealed that extracellular iron accumulation might potentially induce binding of APP to BACE1 for amyloid formation and decrease the capability of APP/Fpn1 in mediating iron export. Our findings in this study, reflecting a probable relationship between iron dyshomeostasis and amyloid pathology, may help shed light on the underlying pathogenesis of CMBs in vascular cognitive impairment.


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