Книги: "Cerebral arteries"

1

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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2

W, Baumgartner R., ed. Handbook on cerebral artery dissection. Basel: Karger, 2005.

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3

Berguer, Ramon. Surgery of the arteries to the head. New York: Springer-Verlag, 1992.

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4

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

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5

K, Perktold, ed. Computer Simulation lokaler arterieller Strömungsformen unter besonderer Beachtung der cerebralen Gefässe. Graz: Forschungsgesellschaft Joanneum, 1987.

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6

Hajime, Handa, Kikuchi Haruhiko, Yonekawa Yasuhiro 1939-, and International Symposium on Microvascular Anastomoses for Cerebral Ischemia (6th : 1982 : Kyoto, Japan), eds. Microsurgical anastomoses for cerebral ischemia. New York: Igaku-Shoin, 1985.

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7

Noé, Battistini, ed. Acute brain ischemia: Medical and surgical therapy. New York: Raven Press, 1986.

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8

U, Sliwka, and United States. National Aeronautics and Space Administration., eds. Effects of sustained low-level elevations of carbon dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. [Washington, DC: National Aeronautics and Space Administration, 1996.

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9

U, Sliwka, and United States. National Aeronautics and Space Administration., eds. Effects of sustained low-level elevations of carbon dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. [Washington, DC: National Aeronautics and Space Administration, 1996.

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10

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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11

P, Pullicino, Caplan Louis R, and Hommel Marc, eds. Cerebral small artery disease. New York, N.Y: Raven Press, 1993.

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12

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

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13

Breisgau, Universität Freiburg im, ed. Der Einfluss von Halothan und Isofluran auf die Blutfliessgeschwindigkeit in der Arteria cerebri media, gemessen mit der Transkraniellen Dopplersonographie. [s.l.]: [s.n.], 1992.

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14

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

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15

Eugene F. Bernstein MD PhD, Allan D Callow . MD PhD, Andrew N. Nicolaides MD FRCS, and Edward G. Shifrin MD PhD. Cerebral Revascularisation. Med-Orion Publishing Co Ltd, 1993.

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16

How We Plan to Achieve Our Vision. Natl Board for Professional, 1994.

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17

Berguer, Ramon. Surgery of the Arteries to the Head. Springer, 2011.

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18

McCormick, C. W., and S. J. Peerless. Microsurgery for Cerebral Ischemia. Springer, 2012.

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19

Manzardo, L., Edouard Kieffer, and Ramon Berguer. Surgery of the Arteries to the Head. Springer London, Limited, 2012.

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20

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

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21

Brock, M., and H. Dietz. Extra-Intracranial Vascular Anastomoses, Microsurgery at the Edge of the Tentorium (Advances in Neurosurgery). Springer, 1985.

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22

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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23

Widder, Bernhard, and Michael Görtler. Doppler- und Duplexsonographie der hirnversorgenden Arterien. 6th ed. Springer, 2006.

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24

P. Pearse Morris MB BCh. Practical Neuroangiography. LWW, 2013.

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25

Cerebral Protection In Cerebrovascular And Aortic Surgery. STEINKOPFF: DARMSTADT, 1997.

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26

Practical neuroangiography. Baltimore: Williams & Wilkins, 1997.

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27

Practical neuroangiography. 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2007.

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28

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

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29

Lasiaunias, P., and Alejandro Berenstein. Surgical Neuroangiography: Functional Anatomy of Craniofacial Arteries. Springer, 1987.

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30

Berenstein, Alejandro, and Pierre Lasjaunias. Surgical Neuroangiography: 1 Functional Anatomy of Craniofacial Arteries. Springer London, Limited, 2012.

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31

Effects of sustained low-level elevations of carbon dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. [Washington, DC: National Aeronautics and Space Administration, 1996.

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32

Effects of sustained low-level elevations of carbon dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. [Washington, DC: National Aeronautics and Space Administration, 1996.

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33

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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34

Brown, Christina, and Jamie E. Rubin. Moyamoya Disease. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0032.

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Moyamoya is a rare cerebrovascular disorder characterized by progressive stenosis of the large cerebral arteries. Cerebral ischemia is the most common manifestation in the pediatric population and may present with symptoms of headache, hypertension, blindness, and developmental delay. The gold standard for diagnosis of Moyamoya is digital subtraction angiography but less invasive imaging modalities such as magnetic resonance imaging/angiogram or perfusion magnetic resonance imaging are typically used. Progressive disease is usually treated with surgical revascularization. Indirect revascularization procedures are preferred to direct revascularization in children due to small caliber of vessels, but regardless of the surgical procedure performed, patients often have some degree of long-term neurological impairment after surgery. Maintenance of cerebral perfusion pressure is critical during the perioperative period, and the patient must be monitored closely for signs of cerebral ischemia.

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35

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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36

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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37

Harrison, Mark. Central nervous system. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0006.

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This chapter describes the anatomy of the central nervous system as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of the structure, anatomy, and arteries of the cerebral hemispheres, blood supply and venous drainage, brainstem, cerebrospinal fluid, cerebellum, spinal cord, and core blood supply. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.

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38

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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39

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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40

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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41

Spinelli, Allison, and Liang Huang. Arteriovenous Malformation. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0006.

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Arteriovenous malformation (AVM) is an abnormal connection between arteries and veins, bypassing the capillary system, which may occur in the brain or the spinal cord. AVMs are challenging to diagnose, and the symptoms may be subtle or dramatic. The location and extent of the lesion will determine its potential for morbidity as these lesions also affect a young population. Most importantly, the technology and evolution of treatment for AVMs has changed dramatically over the past two decades and now incorporates interventional neuroradiology and stereotactic radiation. Management options include conservative management, surgical resection, endovascular embolization, and stereotactic surgery. This chapter’s discussion will cover surgical and interventional modes of treatment of cerebral AVMs.

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42

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

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43

(Editor), Patrick M. Pullicino, Louis R. Caplan (Editor), and Marc Hommel (Editor), eds. Cerebral Small Artery Disease (Advances in Neurology). Lippincott Williams & Wilkins, 1993.

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44

Sawade, Michael. Dopplerultraschalluntersuchungen zur Funktion der cerebralen Autoregulation sowie aktivitätsbedingter Perfusionsänderungen im Versorgungsgebiet cerebraler Arterien bei Probanden und Patienten mit Läsionen des Kranialen Sympathikussystems oder Cerebralen Ischämien. 2003.

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45

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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46

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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47

Taveras, J. M., G. B. Bradac, and R. Oberson. Angiography and Computed Tomography in Cerebro-Arterial Occlusive Diseases. Springer London, Limited, 2012.

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48

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

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49

Kreisz-Jaeger, Rosa-Maria. Früh- und Spätprognose der Infarkte der Arteria cerebri posterior. 1995.

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50

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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Книги з теми "Cerebral arteries"

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