scholarly journals Cerebral Small Vessel Disease Biomarkers Detection on MRI-Sensor-Based Image and Deep Learning

Sensors ◽  
2019 ◽  
Vol 19 (11) ◽  
pp. 2573 ◽  
Author(s):  
Yi-Zeng Hsieh ◽  
Yu-Cin Luo ◽  
Chen Pan ◽  
Mu-Chun Su ◽  
Chi-Jen Chen ◽  
...  
Keyword(s):  
Deep Learning ◽  
Blood Vessel ◽  
Cerebrovascular Disease ◽  
Small Vessel Disease ◽  
Brain Mri ◽  
Common Factor ◽  
Small Vessel ◽  
Vascular Lesions ◽  
Small Blood Vessel ◽  
The Brain

Magnetic resonance imaging (MRI) offers the most detailed brain structure image available today; it can identify tiny lesions or cerebral cortical abnormalities. The primary purpose of the procedure is to confirm whether there is structural variation that causes epilepsy, such as hippocampal sclerotherapy, local cerebral cortical dysplasia, and cavernous hemangioma. Cerebrovascular disease, the second most common factor of death in the world, is also the fourth leading cause of death in Taiwan, with cerebrovascular disease having the highest rate of stroke. Among the most common are large vascular atherosclerotic lesions, small vascular lesions, and cardiac emboli. The purpose of this thesis is to establish a computer-aided diagnosis system based on small blood vessel lesions in MRI images, using the method of Convolutional Neural Network and deep learning to analyze brain vascular occlusion by analyzing brain MRI images. Blocks can help clinicians more quickly determine the probability and severity of stroke in patients. We analyzed MRI data from 50 patients, including 30 patients with stroke, 17 patients with occlusion but no stroke, and 3 patients with dementia. This system mainly helps doctors find out whether there are cerebral small vessel lesions in the brain MRI images, and to output the found results into labeled images. The marked contents include the position coordinates of the small blood vessel blockage, the block range, the area size, and if it may cause a stroke. Finally, all the MRI images of the patient are synthesized, showing a 3D display of the small blood vessels in the brain to assist the doctor in making a diagnosis or to provide accurate lesion location for the patient.

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.

Brain MRI in Monogenic Cerebral Small Vessel Diseases: A Practical Handbook

2021 ◽  
Vol 21 ◽  
Author(s):  
Leonardo Ulivi ◽  
Mirco Cosottini ◽  
Gianmichele Migaleddu ◽  
Giovanni Orlandi ◽  
Nicola Giannini ◽  
...  
Keyword(s):  
Genetic Testing ◽  
Next Generation Sequencing ◽  
Small Vessel Disease ◽  
Brain Mri ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Next Generation ◽  
Vessel Disease ◽  
Generation Sequencing ◽  
Cerebral Small Vessel Diseases

: Monogenic cerebral small vessel diseases are a topic of growing interest, as several genes responsible have been recently described and new sequencing techniques such as Next generation sequencing are available. Brain imaging is a key exam in these diseases. First, since it is often the first exam performed, an MRI is key in selecting patients for genetic testing and for interpreting Next generation sequencing reports. In addition, neuroimaging can be helpful in describing the underlying pathological mechanisms involved in cerebral small vessel disease. With this review, we aim to provide Neurologists and Stroke physicians with an up-to date overview of the current neuroimaging knowledge on monogenic small vessel diseases.

Abstract T MP57: Coexisting Cerebrovascular Disease and Risk of Occult Atrial Fibrillation in Patients With Embolic Stroke of Undetermined Source

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Esther Rojo ◽  
María Sandín-Fuentes ◽  
Ana I Calleja ◽  
Gabriel Largaespada ◽  
Elisa Cortijo ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Secondary Prevention ◽  
Cerebrovascular Disease ◽  
Cox Regression ◽  
Small Vessel Disease ◽  
Brain Magnetic Resonance Imaging ◽  
Embolic Stroke ◽  
Small Vessel ◽  
Large Artery ◽  
Vessel Disease

Background and objective: Secondary prevention after embolic stroke of undetermined source (ESUS) remains a clinical problem. Presence of asymptomatic cerebral large-artery atherosclerosis or small vessel disease could be aprioristically taken as an indicator of a lower risk for an occult cardiac source of emboli, thus influencing our secondary prevention strategy. We aimed to study the relationship between presence and degree of coexisting cerebrovascular disease and the risk of occult paroxysmal atrial fibrillation (OPAF) in ESUS patients. Methods: Longitudinal prospective study in patients fulfilling ESUS criteria after complete neurovascular and cardiac diagnostic workup, who were implanted with a subcutaneous REVEAL-XT loop-recorder to detect OPAF and followed-up for≥ 6 months. At baseline, cerebral large-artery atherosclerosis was assessed with cervical and transcranial ultrasound. Brain magnetic resonance imaging was used to evaluate small vessel disease. Periventricular (PV) and subcortical (SC) white matter hiperintensities (WMH) were categorized using the Fazekas score. Results: We studied 136 ESUS patients from October 2010 to December 2013 (71 men, mean age 67), who were followed-up for a mean time of 594 days. OPAF was detected in 56 (41%) of them. No relationship was found between extracranial or intracranial atherosclerosis and OPAF. Kaplan-Meier curves and crude Cox-regression analyses found associations between OPAF risk and age, smoking, CHA2DS2VASC score, presence of lacunar infarctions, and presence and degree of PVWMH & SCWMH. A multivariable-adjusted Cox regression model identified grade 2-3 PVWMH (HR 3.6, [2.0-6.5], p<0.001) and age as independent predictors of OPAF. Conclusion: Coexisting small vessel disease, specifically in the form of periventricular WMH, is a predictor of OPAF in ESUS patients. Presence of large-artery atherosclerosis does not lower the risk for OPAF. Therefore, OPAF should be actively pursued in ESUS patients regardless the coexistence of asymptomatic cerebrovascular disease.

Abstract TP217: Association Between Thrombophilia and Chronic Cerebrovascular Disease in Young Adults With Acute Ischemic Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Marialaura Simonetto ◽  
Sara Shams ◽  
Xian Wu ◽  
Ivan Diaz ◽  
Setareh Salehi Omran ◽  
...  
Keyword(s):  
Young Adults ◽  
Ischemic Stroke ◽  
White Matter ◽  
Cerebrovascular Disease ◽  
Acute Ischemic Stroke ◽  
Brain Mri ◽  
Mean Difference ◽  
Small Vessel ◽  
Robust Estimator ◽  
Multivariable Analyses

Introduction: Thrombophilias are a known cause of acute ischemic stroke (AIS) in the young. We hypothesized that thrombophilias would be associated with an increased burden of chronic cerebrovascular disease in these patients. Methods: We included patients enrolled in the prospective Cornell AcutE Stroke Academic Registry (CAESAR) who were 18-65 years of age, diagnosed with AIS by brain MRI between 2011-2015, and had thrombophilia testing within 6 months of their stroke. The exposure variable was thrombophilia, defined as at least one positive thrombophilia test according to standard criteria. The primary outcome was the total Age-Related White Matter Changes (ARWMC) score (0-15). Secondary outcomes were the Fazekas score (0-3) and the number of chronic small vessel (subcortical) cerebral infarcts. Outcomes were determined by a single radiologist blinded to thrombophilia status using clinically-performed brain MRIs at the time of index stroke. Doubly robust estimator analyses were used to test the association between an underlying thrombophilia and outcomes. Models were adjusted for age, gender, race, and vascular risk factors. Results: Among 177 patients meeting eligibility criteria, mean age was 47 (SD, 10) years and 50% were women. Thrombophilia was detected in 77 patients (44%). The mean total ARWMC score, Fazekas score, and number of chronic small vessel infarcts were 1.90 (SD, 1.74), 0.91 (SD, 0.69), and 0.16 (SD, 0.63) in patients with thrombophilia and 2.16 (SD, 1.64), 1.07 (SD, 0.69) and 0.35 (SD, 0.81) in patients without thrombophilia. In multivariable analyses, there was no difference in the total ARWMC score (mean difference -0.05, 95% CI -0.43 to 0.33, p=0.80) or Fazekas score (mean difference -0.05, 95% CI -0.21 to 0.11, p=0.52) between patients with thrombophilia and those without. However, in multivariable analyses, the number of chronic infarcts (mean difference -0.22, 95% CI -0.42 to -0.01, p=0.01) was lower in patients with thrombophilia than in those without. Conclusions: In a single-center study of young adults with AIS, underlying thrombophilia was not associated with white matter disease burden. However, contrary to our hypothesis, it was inversely associated with the number of chronic small vessel infarcts.

Small vessel disease

2020 ◽  
pp. 203-212
Author(s):  
Fergus N Doubal ◽  
Anna Poggesi ◽  
Leonardo Pantoni ◽  
Joanna M Wardlaw
Keyword(s):  
Small Vessel Disease ◽  
Current Knowledge ◽  
Intrinsic Disorder ◽  
Small Vessel ◽  
Imaging Features ◽  
World Region ◽  
Vessel Disease ◽  
Cerebral Arterioles ◽  
The Brain ◽  
Review Current

‘Small vessel disease’ describes a combination of neuroradiological and clinical features that are due to an intrinsic disorder of the small cerebral arterioles, capillaries, and venules in varying proportions. It is very common, usually sporadic, although rare monogenic forms are well described. The commonest presentations are with stroke or cognitive impairment. The cause of the small vessel abnormalities in the sporadic form is not well understood and the brain damage is generally attributed to ischaemia secondary to the vessel abnormality. However, evidence for altered microvessel function and blood brain barrier failure is accumulating. The commonest risk factors are increasing age, hypertension, smoking, and diabetes, but environmental and lifestyle factors are also important although poorly understood. Whether the imaging features or incidence of small vessel-related stroke or dementia vary by world region is unknown. We review current knowledge on presentation, aetiology, incidence, and prevalence of sporadic small vessel disease.

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