Epidemiology and aetiopathogenesis

2020 ◽  
pp. 9-24
Author(s):  
Timothy J. England
Keyword(s):  
Small Vessel Disease ◽  
The Elderly ◽  
Developed Countries ◽  
Amyloid Angiopathy ◽  
Ageing Population ◽  
Vessel Disease ◽  
The Brain ◽  
Spontaneous Intracerebral Haemorrhage ◽  
Pathological Subtypes ◽  
Large Vessel Disease

Stroke is a common disabling condition associated with a high mortality, especially in the elderly. Subsequent social and monetary costs are high and despite a decreasing incidence of stroke in developed countries in recent years, prevalence has not declined due to an ageing population. Chapter 2 deals with ‘Epidemiology and aetiopathogenesis’ and examines the definitions of stroke and its pathological subtypes; epidemiology on a worldwide basis; age-specific data; mortality rates; cerebral blood flow and its relationship with ischaemic thresholds; and macroscopic and microscopic changes in the brain with increasing age and their relationship with ischaemic and haemorrhagic strokes. Changes related to large vessel disease, cardioembolism, small vessel disease, inflammatory arteriopathies, spontaneous intracerebral haemorrhage and cerebral amyloid angiopathy, are also described.

Experimental Rodent Models of Vascular Dementia: A Systematic Review

2021 ◽  
Vol 19 ◽  
Author(s):  
Nidhi Tiwari ◽  
Jyoti Upadhyay ◽  
Mohd Nazam Ansari ◽  
Syed Shadab Raza ◽  
Wasim Ahmad ◽  
...  
Keyword(s):  
Vascular Dementia ◽  
Small Vessel Disease ◽  
Current Knowledge ◽  
Vascular Cognitive Impairment ◽  
Experimental Models ◽  
New Drugs ◽  
Amyloid Angiopathy ◽  
Vessel Disease ◽  
The Brain ◽  
Large Vessel Disease

: Vascular dementia (VaD) occurs due to cerebrovascular insufficiency, which leads to decreased blood circulation to the brain, thereby resulting in mental disabilities. The main causes of vascular cognitive impairment (VCI) are severe hypoperfusion, stroke, hypertension, large vessel disease (cortical), small vessel disease (subcortical VaD), strategic infarct, hemorrhage (microbleed), cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), and cerebral amyloid angiopathy (CAA),which leads to decreased cerebrovascular perfusion. Many metabolic disorders such as diabetes mellitus (DM), dyslipidemia, and hyperhomocysteinemia are also related to VaD. The rodent experimental models provide a better prospective for the investigation of the molecular mechanism of new drugs. A plethora of experimental models are available that mimic the pathological conditions and lead to VaD. This review article updates the current knowledge on the basis of VaD, risk factors, pathophysiology, mechanism, advantages, limitations, and the modification of various available rodent experimental models.

scholarly journals High On-Treatment Platelet Reactivity Affects the Extent of Ischemic Lesions in Stroke Patients Due to Large-Vessel Disease

2020 ◽  
Vol 9 (1) ◽  
pp. 251 ◽  
Author(s):  
Adam Wiśniewski ◽  
Joanna Sikora ◽  
Agata Sławińska ◽  
Karolina Filipska ◽  
Aleksandra Karczmarska-Wódzka ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Small Vessel Disease ◽  
Platelet Reactivity ◽  
Volume Measurement ◽  
Large Vessel ◽  
Vessel Disease ◽  
Fluid Attenuated Inversion Recovery ◽  
The Brain ◽  
Large Vessel Disease

Background: Excessive platelet activation and aggregation plays an important role in the pathogenesis of ischemic stroke. Correlation between platelet reactivity and ischemic lesions in the brain shows contradictory results and there are not enough data about the potential role of stroke etiology and its relationships with chronic lesions. The aim of this study is to assess the relationship between platelet reactivity and the extent of ischemic lesions with the particular role of etiopathogenesis. Methods: The study involved 69 patients with ischemic stroke, including 20 patients with large-vessel disease and 49 patients with small-vessel disease. Evaluation of platelet reactivity was performed within 24 h after the onset of stroke using two aggregometric methods (impedance and optical), while ischemic volume measurement in the brain was performed using magnetic resonance imaging (in diffusion-weighted imaging (DWI) and fluid-attenuated inversion recovery (FLAIR) sequences) at day 2–5 after the onset of stroke. Results: In the large-vessel disease subgroup, a correlation was found between platelet reactivity and acute ischemic focus volume (correlation coefficient (R) = 0.6858 and p = 0.0068 for DWI; R = 0.6064 and p = 0.0215 for FLAIR). Aspirin-resistant subjects were significantly more likely to have a large ischemic focus (Odds Ratio (OR) = 45.00, 95% Confidence Interval (CI) = 1.49–135.36, p = 0.0285 for DWI; OR = 28.00, 95% CI = 1.35–58.59, p = 0.0312 for FLAIR) than aspirin-sensitive subjects with large-vessel disease. Conclusion: In patients with ischemic stroke due to large-vessel disease, high on-treatment platelet reactivity affects the extent of acute and chronic ischemic lesions.

scholarly journals Cerebral Small Vessel Disease and Cerebral Amyloid Angiopathy

2019 ◽  
Author(s):  
Raffaella Valenti
Keyword(s):  
Cognitive Rehabilitation ◽  
Small Vessel Disease ◽  
Prognostic Significance ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Elderly Subjects ◽  
Amyloid Angiopathy ◽  
Vessel Disease ◽  
Cerebral Amyloid ◽  
The Brain

Sporadic cerebral small vessel disease (SVD) is considered to be among the most commonly known neuropathological processes in the brain, hosting a crucial role in stroke, cognitive impairment, and functional loss in elderly subjects. We investigated clinical (neuroimaging and cognitive) biomarkers in the SVD, through a series of analyses from our five studies. Sporadic cerebral SVD is a complex ‘micro-world’ to be globally considered. All the relevant lesion types and SVD neuroimaging burden should be taken into account. The cumulative effects of microangiopathy burden in the brain of patients affected by SVD are crucial. Cognitive rehabilitation could represent a promising approach to prevent vascular dementia or to improve cognitive performances in patients with cerebral SVD. Longitudinal studies may provide more robust information about the progression and prognostic significance of our findings.

LDL phenotype B and other lipid abnormalities in patients with large vessel disease and small vessel disease

2003 ◽  
Vol 214 (1-2) ◽  
pp. 11-16 ◽  
Author(s):  
Agnieszka Slowik ◽  
Tomasz Iskra ◽  
Wojciech Turaj ◽  
Jadwiga Hartwich ◽  
Aldona Dembinska-Kiec ◽  
...  
Keyword(s):  
Small Vessel Disease ◽  
Large Vessel ◽  
Small Vessel ◽  
Vessel Disease ◽  
Lipid Abnormalities ◽  
Large Vessel Disease

scholarly journals Role of Purinergic Signalling in Endothelial Dysfunction and Thrombo-Inflammation in Ischaemic Stroke and Cerebral Small Vessel Disease

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 994
Author(s):  
Natasha Ting Lee ◽  
Lin Kooi Ong ◽  
Prajwal Gyawali ◽  
Che Mohd Nasril Che Mohd Nassir ◽  
Muzaimi Mustapha ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Inflammatory Response ◽  
Small Vessel Disease ◽  
Ischemia Reperfusion ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Purinergic Signalling ◽  
Vessel Disease ◽  
The Brain

The cerebral endothelium is an active interface between blood and the central nervous system. In addition to being a physical barrier between the blood and the brain, the endothelium also actively regulates metabolic homeostasis, vascular tone and permeability, coagulation, and movement of immune cells. Being part of the blood–brain barrier, endothelial cells of the brain have specialized morphology, physiology, and phenotypes due to their unique microenvironment. Known cardiovascular risk factors facilitate cerebral endothelial dysfunction, leading to impaired vasodilation, an aggravated inflammatory response, as well as increased oxidative stress and vascular proliferation. This culminates in the thrombo-inflammatory response, an underlying cause of ischemic stroke and cerebral small vessel disease (CSVD). These events are further exacerbated when blood flow is returned to the brain after a period of ischemia, a phenomenon termed ischemia-reperfusion injury. Purinergic signaling is an endogenous molecular pathway in which the enzymes CD39 and CD73 catabolize extracellular adenosine triphosphate (eATP) to adenosine. After ischemia and CSVD, eATP is released from dying neurons as a damage molecule, triggering thrombosis and inflammation. In contrast, adenosine is anti-thrombotic, protects against oxidative stress, and suppresses the immune response. Evidently, therapies that promote adenosine generation or boost CD39 activity at the site of endothelial injury have promising benefits in the context of atherothrombotic stroke and can be extended to current CSVD known pathomechanisms. Here, we have reviewed the rationale and benefits of CD39 and CD39 therapies to treat endothelial dysfunction in the brain.

Physiology and Clinical Relevance of Enlarged Perivascular Spaces in the Aging Brain

Neurology ◽  
2021 ◽  
pp. 10.1212/WNL.0000000000013077
Author(s):  
Corey W Bown ◽  
Roxana O Carare ◽  
Matthew S Schrag ◽  
Angela L Jefferson
Keyword(s):  
Fluid Transport ◽  
Small Vessel Disease ◽  
Treatment Strategies ◽  
Small Vessel ◽  
Aging Brain ◽  
Perivascular Spaces ◽  
Vessel Disease ◽  
Clinical Consequences ◽  
The Brain

Perivascular spaces (PVS) are fluid filled compartments that are part of the cerebral blood vessel wall and represent the conduit for fluid transport in and out of the brain. PVS are considered pathologic when sufficiently enlarged to be visible on magnetic resonance imaging. Recent studies have demonstrated that enlarged PVS (ePVS) may have clinical consequences related to cognition. Emerging literature points to arterial stiffening and abnormal protein aggregation in vessel walls as two possible mechanisms that drive ePVS formation. In this review, we describe the clinical consequences, anatomy, fluid dynamics, physiology, risk factors, and in vivo quantification methods of ePVS. Given competing views of PVS physiology, we detail the two most prominent theoretical views and review ePVS associations with other common small vessel disease markers. As ePVS are a marker of small vessel disease and ePVS burden is higher in Alzheimer’s disease, a comprehensive understanding about ePVS is essential in developing prevention and treatment strategies.

scholarly journals Response to "Carotid Flow Augmentation as a Risk for Small Vessel Disease of the Brain"

2010 ◽  
Vol 23 (9) ◽  
pp. 933-933
Author(s):  
K. Kohara ◽  
N. Ochi ◽  
Y. Tabara ◽  
T. Miki
Keyword(s):  
Small Vessel Disease ◽  
Small Vessel ◽  
Vessel Disease ◽  
The Brain ◽  
Carotid Flow

scholarly journals Risk factors for small-vessel disease revealed by magnetic resonance imaging of the brain.

Nosotchu ◽  
1996 ◽  
Vol 18 (1) ◽  
pp. 10-18
Author(s):  
Tatsuo Kohriyama ◽  
Shinya Yamaguchi ◽  
Eiji Tanaka ◽  
Yasuhiro Yamamura ◽  
Shigenobu Nakamura
Keyword(s):  
Magnetic Resonance Imaging ◽  
Risk Factors ◽  
Magnetic Resonance ◽  
Small Vessel Disease ◽  
Small Vessel ◽  
Resonance Imaging ◽  
Vessel Disease ◽  
The Brain

scholarly journals Potassium channelopathy-like defect underlies early-stage cerebrovascular dysfunction in a genetic model of small vessel disease

2015 ◽  
Vol 112 (7) ◽  
pp. E796-E805 ◽  
Author(s):  
Fabrice Dabertrand ◽  
Christel Krøigaard ◽  
Adrian D. Bonev ◽  
Emmanuel Cognat ◽  
Thomas Dalsgaard ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Genetic Model ◽  
Small Vessel Disease ◽  
Early Stage ◽  
Mesenteric Arteries ◽  
Small Vessel ◽  
Pial Arteries ◽  
Vessel Disease ◽  
Myogenic Responses ◽  
The Brain

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), caused by dominant mutations in the NOTCH3 receptor in vascular smooth muscle, is a genetic paradigm of small vessel disease (SVD) of the brain. Recent studies using transgenic (Tg)Notch3R169C mice, a genetic model of CADASIL, revealed functional defects in cerebral (pial) arteries on the surface of the brain at an early stage of disease progression. Here, using parenchymal arterioles (PAs) from within the brain, we determined the molecular mechanism underlying the early functional deficits associated with this Notch3 mutation. At physiological pressure (40 mmHg), smooth muscle membrane potential depolarization and constriction to pressure (myogenic tone) were blunted in PAs from TgNotch3R169C mice. This effect was associated with an ∼60% increase in the number of voltage-gated potassium (KV) channels, which oppose pressure-induced depolarization. Inhibition of KV1 channels with 4-aminopyridine (4-AP) or treatment with the epidermal growth factor receptor agonist heparin-binding EGF (HB-EGF), which promotes KV1 channel endocytosis, reduced KV current density and restored myogenic responses in PAs from TgNotch3R169C mice, whereas pharmacological inhibition of other major vasodilatory influences had no effect. KV1 currents and myogenic responses were similarly altered in pial arteries from TgNotch3R169C mice, but not in mesenteric arteries. Interestingly, HB-EGF had no effect on mesenteric arteries, suggesting a possible mechanistic basis for the exclusive cerebrovascular manifestation of CADASIL. Collectively, our results indicate that increasing the number of KV1 channels in cerebral smooth muscle produces a mutant vascular phenotype akin to a channelopathy in a genetic model of SVD.

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