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Books on the topic 'Cerebral Arteriole'

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Published: 4 June 2021
Last updated: 1 February 2022

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1

1930-, Bevan John A., ed. Arterial behavior and blood circulation in the brain. New York: Consultants Bureau, 1986.

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2

Ultrasound diagnosis of cerebrovascular disease: Doppler sonography of the extra- and intracranial arteries duplex scanning. Stuttgart: Georg Thieme Verlag, 1993.

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3

Neurovascular imaging: MRI & microangiography. Dordrecht: Springer, 2010.

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4

Takahashi, Shōki. Neurovascular imaging: MRI & microangiography. Dordrecht: Springer, 2010.

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5

N, Tulenko Thomas, and Cox Robert H, eds. Recent advances in arterial diseases: Atherosclerosis, hypertension, and vasospasm : proceedings of the A.N. Richards Symposium, held in Philadelphia, Pennsylvania, May 10-11, 1984. New York: Liss, 1986.

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6

Schieuink. Cerebral and cervical Arterial Dissections. Dunitz Martin Ltd, 2004.

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7

Fisch, Adam. Arterial Supply. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199845712.003.0251.

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Chapter 19 discusses arterial supply, including the Circle of Willis, leptomeningeal cerebral arteries, deep cerebral arteries, arterial border zones, and arteries of the brainstem, cerebellum, spinal cord, and thalamus.
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8

Markus, Hugh, Anthony Pereira, and Geoffrey Cloud. Cerebral venous thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198737889.003.0012.

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Most stroke results from arterial disease but venous occlusion can also cause stroke, and other neurological complications. This condition is uncommon and needs a high index of suspicion if it is not to be missed. The clinical presentations are varied and can mimic other neurological conditions. The diagnosis is important because with appropriate treatment the prognosis can be much better than for arterial infarction.
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9

Perez, Victor Hugo. Atlas Del Sistema Arterial Cerebral Con Variantes Anatomicas. Editorial Limusa S.A. De C.V., 2002.

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10

De Deyne, Cathy, Ward Eertmans, and Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0016_update_001.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables—with possible impact on optimal cerebral perfusion/oxygenation—such as invasive arterial blood pressure monitoring or arterial blood gas analysis.
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11

De Deyne, Cathy, and Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0016.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables such as invasive arterial blood pressure monitoring or arterial blood gas analysis.
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12

Bradac, G. B., and R. Oberson. Angiography and Computed Tomography in Cerebro-Arterial Occlusive Diseases. Springer, 2011.

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13

Whittle, Ian. Raised intracranial pressure, cerebral oedema, and hydrocephalus. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0604.

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The brain is protected by the cranial skeleton. Within the intracranial compartment are also cerebrospinal fluid, CSF, and the blood contained within the brain vessels. These intracranial components are in dynamic equilibrium due to the pulsations of the heart and the respiratory regulated return of venous blood from the brain. Normally the mean arterial blood pressure, systemic venous pressure, and brain volume are regulated to maintain physiological values for intracranial pressure, ICP. There are a range of very common disorders such as stroke, and much less common, such as idiopathic intracranial hypertension, that are associated with major disturbances of intracranial pressure dynamics. In some of these the contribution to pathophysiology is relatively minor whereas in others it may be substantial and be a major contributory factor to morbidity or even death.Intracranial pressure can be disordered because of brain oedema, disturbances in CSF flow, mass lesions, and vascular engorgement of the brain. Each of these may have variable causes and there may be interactions between mechanisms. In this chapter the normal regulation of intracranial pressure is outlined and some common disease states in clinical neurological practice that are characterized by either primary or secondary problems in intracranial pressure dynamics described.
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14

Courbier. Basis Class Cerebral Arterial Disease: Proceedings of a Symposium held in Marseilles, 28-29 September 1984. Excerpta Medica, 1985.

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15

Chappell, Michael, Bradley MacIntosh, and Thomas Okell. Introduction to Perfusion Quantification using Arterial Spin Labelling. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198793816.001.0001.

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Arterial spin labeling (ASL) magnetic resonance imaging (MRI) is unique in being a completely non-invasive method for imaging perfusion in the brain. Relying upon a blood-borne tracer that is created by the MRI scanner itself, ASL is becoming a popular tool to study cerebral perfusion, as well as how this perfusion changes in response to neuronal activity or in disease. This primer provides an introduction to perfusion quantification using ASL MRI, focusing both on the methods needed to extract perfusion-weighted images and on how to quantify perfusion and other hemodynamic parameters. Starting with the simplest implementation of ASL, the primer details all the common acquisition methods, as well as the subsequent analysis steps required to quantify perfusion in an individual, detect changes in perfusion in response to neural activity or pharmacological intervention, and examine perfusion variations across groups of individuals. This is supported with examples from real data illustrating all the major steps in the analysis process, linked to online material where the reader can undertake the same analysis for themselves.
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16

Robert, Courbier, ed. Basis for a classification of cerebral arterial diseases: Proceedings of a symposium held in Marseilles, 28-29 September 1984. Amsterdam: Excerpta Medica, 1985.

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17

Brada?, Gianni Boris. Angiography in Cerebro-Arterial Occlusive Diseases: Including Computer Tomography and Radionuclide Methods. Springer, 2012.

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18

Markus, Hugh, Anthony Pereira, and Geoffrey Cloud. Vascular anatomy and stroke syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198737889.003.0003.

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Determining the arterial territory in which a stroke occurs is important in diagnosis. It also has major implications for management; for example, treatment of a symptomatic carotid stenosis differs greatly to that of an incidental stenosis in a patient with posterior circulation stroke. This chapter describes the arterial supply of the brain and links it to stroke syndromes that present acutely to the stroke clinician. It also covers the venous supply which is important in understanding cerebral venous thrombosis.
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19

Pisklakov, Sergey, Haitham Ibrahim, and Ingrid A. Fitz-James Antoine. Elevated ICP. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0023.

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Perioperative management of a patient with elevated intracranial pressure (ICP) is of paramount importance in neuroanesthesiology. Should this clinical emergency remain unaddressed, disability and death will ensue. Suboptimal care of a patient with elevated ICP is associated with avoidable morbidity and predictable mortality unless timely medical interventions, a focused history, targeted physical findings and a high degree of clinical suspicion confirmed by selective imaging result in medical stabilization and more definitive neurosurgical intervention. This may require interinstitutional transport. Understanding the physiologic and pathologic concepts that underlie elevated ICP permit anticipatory interventions to avert inexorable deterioration. The etiology of elevated intracranial pressure is often multifactorial. The deleterious effects of rising ICP demand a clear understanding of the relationship between ICP, mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and cerebral autoregulation. Maintaining optimal CPP to prevent cerebral ischemia is the neuroanesthesiologist’s ultimate goal while managing a patient with an elevated ICP.
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20

S, Kim Jong, Caplan Louis R, and Wong K. S. Lawrence, eds. Intracranial atherosclerosis. Chichester: Wiley-Blackwell, 2008.

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21

Caplan, Louis R., Jong S. Kim, and K. S. Lawrence Wong. Intracranial Atherosclerosis. Wiley & Sons, Incorporated, John, 2009.

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22

Crum, Brian A., Eduardo E. Benarroch, and Robert D. Brown. Neurologic Disorders Categorized by Mechanism. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0524.

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Mechanisms of neurologic disease can be cerebrovascular, neoplastic, movement disorders, infectious diseases. The causes of ischemic cerebrovascular disorders can be classified on the basis of the site of the source for the arterial blockage within the vascular system, from most proximal to distal. The causes of ischemic cerebrovascular disorders, including transient ischemic attack and cerebral infarction, can be classified on the basis of the site of the source for the arterial blockage within the vascular system, from most proximal to distal. Tremor is an oscillatory rhythmic movement disorder. A simple classification of tremor is rest tremor and action tremor. Infectious diseases of the nervous system are manifested in various combinations of meningitis, encephalitis, brain abscess, granulomas, and vasculitis.
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23

Chappell, Michael, Bradley MacIntosh, and Thomas Okell. Partial Volume Effects. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198793816.003.0006.

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Partial volume effects are present in all medical imaging methods, and they play a specific role in arterial spin labeling (ASL) MRI measurements of perfusion. This chapter demonstrates how differences in the perfusion properties of gray matter, white matter, and cerebrospinal fluid give rise to the distinctive visual appearance of cerebral perfusion images. The implications of this for quantification of perfusion in gray matter are discussed and solutions to correct for partial volume effects presented.
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24

Leira, Enrique C. Unusual Causes of Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0105.

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Unusual causes of stroke include those etiologies of cerebral infarction that are not related to the most common mechanisms of atherosclerosis or cardioembolism. This category includes non-atherosclerotic arteriopathies such as arterial dissection, moyamoya, and central nervous system (CNS) vasculitis. It also includes strokes related to a hypercoagulable state. Because the prevalence of atherosclerosis increases with age, unusual causes of stroke are more commonly seen in younger individuals in whom stroke is often not suspected, and therefore not readily diagnosed. Due to the relative rarity, these patients are difficult to test in clinical trials, which makes progress in management challenging.
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25

Chappell, Michael, Bradley MacIntosh, and Thomas Okell. Introduction. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198793816.003.0001.

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This chapter details the widely accepted standard approach to arterial spin labeling (ASL) acquisition and the associated analysis needed to extract an image of perfusion in the brain, also known as the cerebral blood flow (CBF). Starting with pairs of images with and without labeling, a perfusion-weighted image can be generated. With the addition of a calibration image, this can be converted to an absolute measure of perfusion. Following the recommendations of the community for ASL acquisition, this chapter outlines the main steps of subtraction, kinetic model inversion, and calibration required for analysis of ASL data.
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26

Recent advances in arterial diseases: Atherosclerosis, hypertension, and vasospasm : Proceedings of the A.N. Richards Symposium, held in Philadelphia, ... in clinical and biological research). Liss, 1986.

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27

Langer, Thomas, and Pietro Caironi. Pathophysiology and therapeutic strategy of respiratory alkalosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0114.

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Respiratory alkalosis is a condition characterized by low partial pressure of carbon dioxide and an associated elevation in arterial pH caused by an imbalance between CO2 production and removal, in favour of the latter. Conditions that cause increased alveolar ventilation, without having a reduction in pH as input stimulus, will cause hypocapnia associated with a variable degree of alkalosis. The major effect of hypocapnia is the increase in pH (alkalosis) and the consequent shift of electrolytes that occurs in relation to it. As a general law, in plasma, anions will increase, while cations will decrease. The acute reduction in ionized calcium, due to the change in extracellular pH, may cause neuromuscular symptoms ranging from paraesthesias, to tetany and seizures. The effect on urine is an increase in urinary strong ion difference/urinary anion gap and a consequent increase in urinary pH. Finally, acute hypocapnic alkalosis causes a constriction of cerebral arteries that can lead to a reduction of cerebral blood flow. The clinical approach to respiratory alkalosis is usually directed toward the diagnosis and treatment of the underlying clinical disorder.
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28

Waldmann, Carl, Neil Soni, and Andrew Rhodes. Obstetric emergencies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0031.

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Pre-eclampsia 518Eclampsia 520HELLP syndrome 522Postpartum haemorrhage 524Amniotic fluid embolism 526Pre-eclampsia is a common complication of pregnancy, UK incidence is 3–5%, with a complex hereditary, immunological and environmental aetiology.Abnormal placentation is characterized by impaired myometrial spiral artery relaxation, failure of trophoblastic invasion of these arterial walls and blockage of some vessels with fibrin, platelets and lipid-laden macrophages. There is a 30–40%, reduction in placental perfusion by the uterine arcuate arteries as seen by Doppler studies at 18–24 weeks gestation. Ultimately the shrunken, calcified, and microembolized placenta typical of the disease is seen. The placental lesion is responsible for fetal growth retardation and increased risks of premature labour, abruption and fetal demise. Maternal systemic features of this condition are characterized by widespread endothelial damage, affecting the peripheral, renal, hepatic, cerebral, and pulmonary vasculatures. These manifest clinically as hypertension, proteinuria and peripheral oedema, and in severe cases as eclamptic convulsions, cerebral haemorrhage (the most common cause of death due to pre-eclampsia in the UK), pulmonary oedema, hepatic infarcts and haemorrhage, coagulopathy and renal dysfunction....
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29

Mathews, Letha, and John Barwise. Refractory Intracranial Hypertension. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0067.

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Intracranial pressure remains constant in adults at 10–15 mmHg under normal conditions with some fluctuations associated with respirations, coughing, sneezing, and so forth. Refractory intracranial hypertension (ICH) is defined by recurrent episodes of intracranial pressure elevation above 20 mmHg for sustained periods (10–15 min) despite medical therapy. The common causes of ICH are traumatic brain injury, brain tumors, subarachnoid hemorrhage, and brain infarction from arterial occlusion, cerebral venous thrombosis, and anoxic encephalopathy. Intracranial infections, abscesses, acute liver encephalopathy, and idiopathic ICH are also recognized causes of ICH. For the purposes of this chapter, the discussion is limited to ICH related to traumatic brain injury.
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30

Saasouh, Wael, and David E. Traul. Extracranial-Intracranial Bypass. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0010.

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Extracranial-intracranial (EC-IC) bypass is a surgical procedure used to preserve or rescue cerebral circulation when the arterial supply is disrupted. There are several techniques of EC-IC bypass depending on the location of the anomaly and the vessels involved, the purpose being to provide a connection from a patent extracranial artery to an artery within the cranium, thus bypassing the anomalic or thrombosed portion. The mainstay of the anesthetic management of this procedure includes careful preoperative evaluation, meticulous intraoperative management, and close postoperative observation. Intracranial bleeding and hyperperfusion after the procedure are the two principal concerns, and proper management strategies should be in place for all cases.
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31

Michel, Jean-Baptiste. Biology of vascular wall dilation and rupture. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0016.

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Arterial pathologies, important causes of death and morbidity in humans, are closely related to modifications in the circulatory system during evolution. With increasing intraluminal pressure and arterial bifurcation density, the arterial wall becomes the target of interactions with blood components and outward convection of plasma solutes and particles, including plasma zymogens and leukocyte proteases. Abdominal aortic aneurysms of atherothrombotic origin are characterized by the presence of an intraluminal thrombus (ILT), a major source of proteases, including plasmin, MMP-9, and elastase. Saccular cerebral aneurysms are characterized by the interaction of haemodynamics and arterial bifurcation defects, of either genetic or congenital origin. They also develop an intrasaccular thrombus, implicated in rupture. Aneurysms of the ascending aorta (TAAs) are not linked to atherothrombotic disease, and do not develop an ILT. The most common denominator of TAAs, whatever their aetiology, is the presence of areas of mucoid degeneration, and increased convection and vSMC-dependent activation of plasma zymogens within the wall, causing extracellular matrix proteolysis. TAA development is also associated with an epigenetic phenomenon of SMAD2 overexpression and nuclear translocation, potentially linked to chronic changes in mechanotransduction. Aortic dissections share common aetiologies and pathology (areas of mucoid degeneration) with TAAs, but differ by the absence of any compensatory epigenetic response. There are main experimental animal models of aneurysms, all characterized by the cessation of aneurysmal progression after interruption of the exogenous stimuli used to induce it. These new pathophysiological approaches to aneurysms in humans pave the way for new diagnostic and therapeutic tools.
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32

Jabbour, Pascal, and Eric Peterson, eds. Radial Access for Neurointervention. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197524176.001.0001.

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Although femoral artery catheterization has been the mainstay of arterial access for cerebral angiography, there has been a recent increase in the use of transradial access among neurointerventionalists. Despite its widespread use among interventional cardiologists, there is a paucity of evidence for its use in the neurosurgical literature. With the constant evolution of device technology and the need of multimodal treatments for complex neurovascular pathologies, most neurointerventionalists resort to femoral artery access because of the vessel’s larger diameter and having been trained with that approach. However, transradial access confers a number of benefits, most notably lower risk of vascular complications, shorter recovery, and increased patient satisfaction and cost reduction. Femoral artery catheterization requires patients to tolerate a painful and uncomfortable procedure, with associated potential complications such as pseudo-aneurysm formation, retroperitoneal hematoma, and artery occlusion. Compared with groin access, radial artery catheterization has been shown to confer a lower risk of local neurovascular complications and improved quality-of-life metrics. This book is the first of its kind, detailing step by step all the technical nuances of the transradial approach in the neurointerventional world, from diagnostic cerebral angiograms to neurointerventional procedures. This is the perfect book for physicians who decided to make the transition of their practice to transradial.
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33

Mason, Peggy. Following the Nutrients. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0008.

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Consciousness depends on oxygen delivered to the brain by arterial blood. Compromises to this delivery by an increase in intracranial pressure or decrease in available oxygen can produce syncope. The blood supply to the forebrain stems from the internal carotids that serve the anterior circulation. The posterior circulation is fed by the vertebral arteries and supplies blood to the brainstem. Redundancy to the brain’s blood supply is served by anastomoses, a connection between the posterior and anterior circulations, and by the Circle of Willis. The clinical characteristics of common brainstem and cerebral strokes are described. Similarly, the characteristics and clinical prognosis of different types of intracranial bleeds are explained. The text covers mechanisms that normally protect the brain and the consequences of traumatic brain injury that overwhelms these protections. A description of the production and circulation of cerebrospinal fluid allows the student to understand hydrocephalus.
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34

Henzi, Bettina, and Maja Steinlin. Stroke in children. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0013.

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Stroke in children is a rare, but terrifying disease and its lifelong sequelae weigh heavy on patients and families. It is also increasingly recognized as a socioeconomic burden, ongoing for many years after the acute manifestation. There is a significant delay in diagnosis of childhood stroke. This is caused by several factors: lack of awareness among the public and professionals, childhood-specific manifestations, numerous stroke mimics, and last but not least, limited access to emergency neuroimaging for children. Fast stroke recognition tools need adaption to the special needs in children. Childhood arterial ischaemic stroke differs in aetiology from adult stroke with cerebral vasculopathies being the leading cause and cardioembolic aetiology ranking second. However, treatment guidelines are largely based on adult guidelines and expert consensus. Future research has to put emphasis on understanding pathophysiology, defining specific treatment options, and providing evidence for treatment guidelines in paediatric stroke.
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35

Waje-Andreassen, Ulrike, and Nicola Logallo. Vascular imaging: Ultrasound. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0009.

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After computed tomography and computed tomography angiography or magnetic resonance imaging and magnetic resonance angiography at admission, ultrasound is the most important diagnostic tool to confirm angiographic findings and to closely follow-up patients until the clinical situation has stabilized. Thrombolysis and interventional therapy have given transcranial ultrasound a very important role in bedside monitoring of occlusions, collaterals, cerebral haemodynamics, and vasoreactivity. Detection of flow changes in sickle cell disease, circulating emboli, and right-to-left shunts may guide treatment decisions. Sonothrombolysis and targeted drug delivery are today’s research projects for acute treatment by ultrasound. Extracranial cerebrovascular ultrasound is an ‘all-round’ diagnostic tool modifying angiographic results, showing minor arterial wall disease, plaques, and plaque instability. Microembolic signals during scanning may contribute to finding the cause of stroke. In stroke prevention, ultrasound delivers the possibility for staging of arteries and improving targeted intervention. Ultrasound images may also serve as educational tools for patients to underline the need for continuous medical treatment and lifestyle changes, and may improve compliance.
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36

Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.

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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β‎‎‎2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β‎‎‎2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.
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