Vascular Pathology

2018 ◽  
pp. 82-121
Author(s):  
Jean-Jacques Hauw ◽  
Steven K. Feske ◽  
Pierre Amarenco ◽  
Umberto De Girolami
Keyword(s):  
Blood Vessels ◽  
Small Vessel Disease ◽  
Clinical Manifestations ◽  
Vascular Diseases ◽  
Vascular Pathology ◽  
Amyloid Angiopathy ◽  
Hereditary Disorders ◽  
The Central Nervous System ◽  
Subarachnoid Spaces ◽  
Large Groups

The classification of vascular diseases of the central nervous system proposed here considers at first two large groups of entities: large intraparenchymal hemorrhage due to rupture of blood vessels and then, infarction from occlusion of major vessels. The underlying vessel abnormality is discussed, as are the reactions over time of nervous tissue to irreversible injury. Intracranial hemorrhages can also be seen in the context of rupture of vessels, with outpouring of blood into the subarachnoid spaces in cases of ruptured aneurysm or of vascular malformation. Small vessel disease is considered separately, these are instances of lesions affecting the microcirculation; clinical manifestations include dementia, encephalopathies, or multifocal neurologic deficits, the result of multiple microhemorrhages, small infarcts, or both. Vascular diseases affecting the small blood vessels include hypertensive cerebrovascular disease and cerebral amyloid angiopathy. Less common entities include hereditary disorders (i.e., cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and vasculitides).

Neuropathology of Vascular Disease

2013 ◽  
pp. 76-113
Author(s):  
Jean-Jacques Hauw ◽  
Umberto De Girolami ◽  
Harry V. Vinters
Keyword(s):  
Blood Vessels ◽  
Small Vessel Disease ◽  
Vascular Malformations ◽  
Vascular Diseases ◽  
Neurological Deficits ◽  
Amyloid Angiopathy ◽  
Hereditary Disorders ◽  
The Central Nervous System ◽  
Subarachnoid Spaces ◽  
Large Groups

The classification of vascular diseases of the central nervous system followed here first considers two large groups of entities: relatively large intraparenchymal hemorrhage due to rupture of blood vessels and infarction from occlusion of major vessels affecting large areas of the brain. The underlying pathology of the vessels is discussed, as are the reactions of nervous tissue to irreversible injury over time. Intracranial hemorrhages can also be seen in the context of rupture of vessels with outpouring of blood into the subarachnoid spaces, in cases of ruptured aneurysm or vascular malformations. Next we consider small vessel disease, in which the lesions affect the microcirculation and may also cause dementia, encephalopathies, or multifocal neurological deficits, the result of multiple micro-hemorrhages, small infarcts, or both. Vascular diseases affecting the small blood vessels include hypertensive cerebrovascular disease and cerebral amyloid angiopathy. Less common entities include hereditary disorders (i.e., CADASIL) and vasculitides.

Small Vessel Disease: Neuropathology

2003 ◽  
Vol 15 (S1) ◽  
pp. 67-69 ◽  
Author(s):  
David G. Munoz
Keyword(s):  
Blood Vessels ◽  
Small Vessel Disease ◽  
Small Vessel ◽  
Amyloid Angiopathy ◽  
Cerebral Blood Vessels ◽  
Vessel Disease ◽  
Different Populations

Diseases of small cerebral blood vessels are heterogeneous in etiology and manifestations. Lipohyalinosis, venous collagenosis, amyloid angiopathy, and CADASIL affect different populations of blood vessels. Large and small hemorrhages, lacunae, cortical microinfarcts, and leukoaraiosis are the most important consequences of the small vessel angiopathies. Altered permeability as well as ischemia may be involved in the pathogenesis of the latter.

scholarly journals Impaired endothelium-mediated cerebrovascular reactivity promotes anxiety and respiration disorders in mice

2020 ◽  
Vol 117 (3) ◽  
pp. 1753-1761 ◽  
Author(s):  
Jan Wenzel ◽  
Cathrin E. Hansen ◽  
Carla Bettoni ◽  
Miriam A. Vogt ◽  
Beate Lembrich ◽  
...  
Keyword(s):  
Vascular Diseases ◽  
Major Product ◽  
Cerebrovascular Reactivity ◽  
Vascular Pathology ◽  
Normal Brain ◽  
Strong Impact ◽  
Vasoactive Factors ◽  
Normal Brain Function ◽  
The Central Nervous System ◽  
Functional Relevance

Carbon dioxide (CO2), the major product of metabolism, has a strong impact on cerebral blood vessels, a phenomenon known as cerebrovascular reactivity. Several vascular risk factors such as hypertension or diabetes dampen this response, making cerebrovascular reactivity a useful diagnostic marker for incipient vascular pathology, but its functional relevance, if any, is still unclear. Here, we found that GPR4, an endothelial H+ receptor, and endothelial Gαq/11 proteins mediate the CO2/H+ effect on cerebrovascular reactivity in mice. CO2/H+ leads to constriction of vessels in the brainstem area that controls respiration. The consequential washout of CO2, if cerebrovascular reactivity is impaired, reduces respiration. In contrast, CO2 dilates vessels in other brain areas such as the amygdala. Hence, an impaired cerebrovascular reactivity amplifies the CO2 effect on anxiety. Even at atmospheric CO2 concentrations, impaired cerebrovascular reactivity caused longer apneic episodes and more anxiety, indicating that cerebrovascular reactivity is essential for normal brain function. The site-specific reactivity of vessels to CO2 is reflected by regional differences in their gene expression and the release of vasoactive factors from endothelial cells. Our data suggest the central nervous system (CNS) endothelium as a target to treat respiratory and affective disorders associated with vascular diseases.

scholarly journals Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies

2020 ◽  
Vol 21 (11) ◽  
pp. 3862 ◽  
Author(s):  
Jayant Patwa ◽  
Swaran Jeet Singh Flora
Keyword(s):  
Heavy Metals ◽  
Heavy Metal ◽  
Blood Vessels ◽  
Small Vessel Disease ◽  
Vascular Dysfunction ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Amyloid Angiopathy ◽  
Vessel Disease ◽  
Antioxidant Defense Enzymes

Heavy metals are considered a continuous threat to humanity, as they cannot be eradicated. Prolonged exposure to heavy metals/metalloids in humans has been associated with several health risks, including neurodegeneration, vascular dysfunction, metabolic disorders, cancer, etc. Small blood vessels are highly vulnerable to heavy metals as they are directly exposed to the blood circulatory system, which has comparatively higher concentration of heavy metals than other organs. Cerebral small vessel disease (CSVD) is an umbrella term used to describe various pathological processes that affect the cerebral small blood vessels and is accepted as a primary contributor in associated disorders, such as dementia, cognitive disabilities, mood disorder, and ischemic, as well as a hemorrhagic stroke. In this review, we discuss the possible implication of heavy metals/metalloid exposure in CSVD and its associated disorders based on in-vitro, preclinical, and clinical evidences. We briefly discuss the CSVD, prevalence, epidemiology, and risk factors for development such as genetic, traditional, and environmental factors. Toxic effects of specific heavy metal/metalloid intoxication (As, Cd, Pb, Hg, and Cu) in the small vessel associated endothelium and vascular dysfunction too have been reviewed. An attempt has been made to highlight the possible molecular mechanism involved in the pathophysiology, such as oxidative stress, inflammatory pathway, matrix metalloproteinases (MMPs) expression, and amyloid angiopathy in the CSVD and related disorders. Finally, we discussed the role of cellular antioxidant defense enzymes to neutralize the toxic effect, and also highlighted the potential reversal strategies to combat heavy metal-induced vascular changes. In conclusion, heavy metals in small vessels are strongly associated with the development as well as the progression of CSVD. Chelation therapy may be an effective strategy to reduce the toxic metal load and the associated complications.

scholarly journals Cerebral small vessel disease: classification, clinical manifestations, diagnosis, and features of treatment

2019 ◽  
Vol 11 (3S) ◽  
pp. 4-17 ◽  
Author(s):  
A. A. Kulesh ◽  
V. E. Drobakha ◽  
V. V. Shestakov
Keyword(s):  
Hemorrhagic Stroke ◽  
Small Vessel Disease ◽  
Clinical Manifestations ◽  
Cerebrovascular Diseases ◽  
Cerebral Small Vessel Disease ◽  
Point Of View ◽  
Disease Classification ◽  
Small Vessel ◽  
Amyloid Angiopathy ◽  
Vessel Disease

The paper considers the relevance of the problem of cerebral small vessel disease (CSVD) that is an important cause of ischemic and hemorrhagic stroke, associated with the development of cognitive impairment and complications of antithrombotic therapy. It presents briefly the current issues of etiology and pathogenesis of the disease. Sporadic non-amyloid microangiopathy, cerebral amyloid angiopathy, and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) are discussed in detail from the point of view of their clinical presentation, neuroimaging, and features of therapeutic tactics. An algorithm for diagnosing CSVD in patients admitted to hospital for stroke and a differentiated approach to their treatment are proposed. Consideration of the neuroimaging manifestations of CSVD is noted to be necessary for the safe and more effective treatment of patients with cerebrovascular diseases.

scholarly journals The Contribution of Vascular Pathology Toward Cognitive Impairment in Older Individuals with Intermediate Braak Stage Tau Pathology

2020 ◽  
Vol 77 (3) ◽  
pp. 1005-1015 ◽  
Author(s):  
Andrew C. Robinson ◽  
Federico Roncaroli ◽  
Stephen Chew-Graham ◽  
Yvonne S. Davidson ◽  
James Minshull ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
White Matter ◽  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Vascular Pathology ◽  
Cognitively Impaired ◽  
Amyloid Angiopathy ◽  
Braak Stage ◽  
Age Related ◽  
Cerebral Amyloid

Background: The pathological features of Alzheimer’s disease (AD) are well described but little is known as to how both neurodegeneration and vascular changes might interact in causing cognitive impairment. Objective: The present study aims to investigate relationships between vascular and AD pathology in cognitively healthy and cognitively impaired individuals with a particular emphasis on those at intermediate Braak tau stages. Methods: We investigated the interplay between Braak tau stage and measures of vascular pathology as described by the vascular cognitive impairment neuropathology guidelines (VCING) in 185 brains from the Brains for Dementia Research programme and The University of Manchester Longitudinal Study of Cognition in Healthy Old Age. VCING asserts that at least one large (>10 mm) infarct, moderate/severe occipital leptomeningeal cerebral amyloid angiopathy, and moderate/severe arteriosclerosis in occipital white matter accurately predicts the contribution of cerebrovascular pathology to cognitive impairment. Results: We found that the extent of arteriosclerosis in the occipital white matter did not differ between cognitive groups at intermediate (III-IV) Braak stages whereas moderate/severe leptomeningeal occipital cerebral amyloid angiopathy was greater in cognitively impaired than normal individuals at Braak stage III-IV. This finding remained significant after controlling for effects of age, sex, CERAD score, Thal phase, presence/severity of primary age-related tauopathy, presence/severity of limbic-predominant age-related TDP43 encephalopathy and small vessel disease in basal ganglia. Conclusion: Interventions targeting cerebral amyloid angiopathy may contribute to delay the onset of cognitive impairment in individuals with intermediate Alzheimer’s type pathology.

Abstract 94: Prevalence and Distinct Imaging Correlates of Deep Versus Lobar Cerebral Microbleeds: The Atherosclerosis Risk in Communities Study

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jonathan Graff-Radford ◽  
Jeannette Simino ◽  
Thomas H Mosley ◽  
Michael E Griswold ◽  
Beverly G Windham ◽  
...  
Keyword(s):  
Small Vessel Disease ◽  
Multinomial Logistic Regression ◽  
Smoking Status ◽  
The Elderly ◽  
Vascular Pathology ◽  
Amyloid Angiopathy ◽  
Intracranial Volume ◽  
Brain Volumes ◽  
Selection Scheme ◽  
Mri Features

Introduction: Cerebral microbleed (CMB) location may predict underlying pathology. Deep CMBs are more associated with hypertensive vascular disease, while lobar CMBs are more associated with cerebral amyloid angiopathy (CAA). The objective of this study was to determine the neuroimaging pathology associated with CMBs. Methods: We analyzed 1,831 nondemented ARIC participants (mean age=76.3 ±5.3 years, 40% male, 27% black) with 3T MRI scans at the fifth exam (2011-13). We fit multinomial logistic regression models to assess the effect of brain volumes (AD signature region atrophy, total gray matter, frontal, and log 2 -transformed white matter hyperintensities (WMH) volume), infarct frequencies (lacunar, non-lacunar, and total), and APOE (number of ε4 alleles) on CMB location (no, any deep, or lobar only CMBs). Models were weighted for the sample selection scheme and adjusted for age, male, education, hypertension, ever smoking status, diabetes, race-site membership, and estimated intracranial volume (brain volume models only). Results: The frequency of CMBs was 24.1%. A larger WMH volume, greater total infarct frequency, and smaller total grey volume increased the relative risks (RR) of both deep and lobar CMBs compared to no CMBs; increasing the WMH volume also increased the RR of deep to lobar CMBs. Additional lacunar infarcts increased the RR of deep compared to no CMBs, whereas AD signature region atrophy and APOE ε4 homozygosity increased the RR of lobar CMBs. Conclusion: CMBs are a common vascular pathology in the elderly. Deep CMB presence is associated with MRI features of hypertensive small vessel disease, while lobar CMB presence is associated with MRI features of CAA and Alzheimer’s disease.

Evidence for a Blood Ganglion Barrier in the Superior Cervical Ganglion of the Rat

1982 ◽  
Vol 40 ◽  
pp. 204-204
Author(s):  
D. M. DePace
Keyword(s):  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Peripheral Nerves ◽  
Time Schedule ◽  
Transmission Electron ◽  
Cervical Ganglion ◽  
The Central Nervous System ◽  
Cervical Ganglia ◽  
Capillary Circulation ◽  
And Control

The majority of blood vessels in the superior cervical ganglion possess a continuous endothelium with tight junctions. These same features have been associated with the blood brain barrier of the central nervous system and peripheral nerves. These vessels may perform a barrier function between the capillary circulation and the superior cervical ganglion. The permeability of the blood vessels in the superior cervical ganglion of the rat was tested by intravenous injection of horseradish peroxidase (HRP). Three experimental groups of four animals each were given intravenous HRP (Sigma Type II) in a dosage of.08 to.15 mg/gm body weight in.5 ml of.85% saline. The animals were sacrificed at five, ten or 15 minutes following administration of the tracer. Superior cervical ganglia were quickly removed and fixed by immersion in 2.5% glutaraldehyde in Sorenson's.1M phosphate buffer, pH 7.4. Three control animals received,5ml of saline without HRP. These were sacrificed on the same time schedule. Tissues from experimental and control animals were reacted for peroxidase activity and then processed for routine transmission electron microscopy.

The molecular mechanism of mechanotransduction in vascular homeostasis and disease

2020 ◽  
Vol 134 (17) ◽  
pp. 2399-2418
Author(s):  
Yoshito Yamashiro ◽  
Hiromi Yanagisawa
Keyword(s):  
Shear Stress ◽  
Blood Vessels ◽  
Vessel Wall ◽  
Vascular Diseases ◽  
Cell Interactions ◽  
Aortic Aneurysms ◽  
Cyclic Stretch ◽  
Mechanical Stimuli ◽  
Vascular Homeostasis ◽  
Matrix Cell

Abstract Blood vessels are constantly exposed to mechanical stimuli such as shear stress due to flow and pulsatile stretch. The extracellular matrix maintains the structural integrity of the vessel wall and coordinates with a dynamic mechanical environment to provide cues to initiate intracellular signaling pathway(s), thereby changing cellular behaviors and functions. However, the precise role of matrix–cell interactions involved in mechanotransduction during vascular homeostasis and disease development remains to be fully determined. In this review, we introduce hemodynamics forces in blood vessels and the initial sensors of mechanical stimuli, including cell–cell junctional molecules, G-protein-coupled receptors (GPCRs), multiple ion channels, and a variety of small GTPases. We then highlight the molecular mechanotransduction events in the vessel wall triggered by laminar shear stress (LSS) and disturbed shear stress (DSS) on vascular endothelial cells (ECs), and cyclic stretch in ECs and vascular smooth muscle cells (SMCs)—both of which activate several key transcription factors. Finally, we provide a recent overview of matrix–cell interactions and mechanotransduction centered on fibronectin in ECs and thrombospondin-1 in SMCs. The results of this review suggest that abnormal mechanical cues or altered responses to mechanical stimuli in EC and SMCs serve as the molecular basis of vascular diseases such as atherosclerosis, hypertension and aortic aneurysms. Collecting evidence and advancing knowledge on the mechanotransduction in the vessel wall can lead to a new direction of therapeutic interventions for vascular diseases.

Clinical Manifestations and Radiological Characteristics on Rosai-Dorfman Disease: A Retrospective Observational Study

2020 ◽  
Vol 5 (5) ◽  
Keyword(s):  
Blood Vessels ◽  
Abdominal Cavity ◽  
Clinical Manifestations ◽  
Ct Images ◽  
High Signal ◽  
Radiological Features ◽  
Imaging Characteristics ◽  
Rosai Dorfman Disease ◽  
Heterogeneous Enhancement ◽  
The Masses

Background and Objective: Rosai-Dorfman disease (RDD) are usually misdiagnosed because of rarity and nonspecific clinical and radiological features. The aim of our study is to explore the clinical and imaging characteristics of RDD to improve diagnostic accuracy. Methods: Clinical and imaging data in 10 patients with RDD were retrospectively analyzed. 7 patients were underwent CT scanning and 3 patients were underwent MR examination. Results: 8 (8/10) patients presented with painless enlarged lymph nodes (LNs) or mass. 3 cases were involved with LNs, 5 cases were involved with extra-nodal tissues, and the remaining 2 cases were involved with LNs and extra-nodal tissue simultaneously. In enhanced CT images, enlarged LNs displayed mild or moderate enhancement, and 2 cases showed heterogeneous ring-enhancement. MR features of 3 patients with extra-nodal RDD, 2 cases showed a mass located in the subcutaneous and anterior abdominal wall respectively, and 1 case showed an intracranial mass. Besides, all lesions showed high signal foci on DWI images, and were characterized by marked heterogeneous enhancement with blurred edge. The dural/fascia tail sign and dilated blood vessels could be seen around all the lesions on enhanced MRI. Radiological features of 2 cases with LN and extranodal tissue involved, one case presented with the swelling and thickening of pharyngeal lymphoid ring and nasopharynx, meanwhile with enlarged LNs in bilateral submandibular area, neck and abdominal cavity, and also companied with osteolytic lesion in right proximal humerus. All these LNs displayed mild and moderate enhancement on CT images. Another case showed enlarged LNs in bilateral neck accompanied with soft tissue mass in the sinuses. Conclusions: RDD occurred commonly in young and middle-aged men and presented with painless enlarged LNs or mass.RDD had a huge diversity of imaging findings, which varied with different location. The radiological features, such as small patches of high signal foci in the masses on DWI images, heterogeneous enhancement and blood vessels around the masses, are helpful in diagnosis of extranodal RDD.

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