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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 28 stycznia 2023

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1

Treatment of cerebral infarction: Experimental and clinical study. Wien: Springer-Verlag, 1987.

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2

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

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3

1931-, Robertson James T., Nowak Thaddeus S i Princeton Conference on Cerebrovascular Disease (20th : 1996 : Memphis, Tenn.), red. Frontiers in cerebrovascular disease: Mechanisms, diagnosis, and treatment. Armonk, NY: Futura Pub. Co., 1998.

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4

M, Maier Carolina, i Steinberg Gary K, red. Hypothermia and cerebral ischemia: Mechanisms and clinical applications. Totowa, N.J: Humana Press, 2004.

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5

Eric, Kasner Scott, i Gorelick Philip B, red. Prevention and treatment of ischemic stroke. Philadelphia: Butterworth-Heinemann, 2004.

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6

1946-, Feuerstein Giora Z., red. Inflammation and stroke. Basel: Birkhäuser, 2001.

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7

M, Barnett Henry J., i Hachinski Vladimir, red. Cerebral ischemia: Treatment and prevention. Philadelphia: Saunders, 1992.

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8

Therapeutic Strategies In Cerebral Ischemia. Clinical Pub, 2011.

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9

R, Caplan Louis, red. Brain ischemia: From basic science to treatment. London: Springer-Verlag, 1994.

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10

(Editor), J. Bogousslavsky, D. Guez (Editor) i Jose Biller (Editor), red. Cerebral Ischemia: From Pathophysiology to Treatment - Journal: Cerebrovascular Diseases, Suppl. 1, 1991 (Cerebral Ischemia). S. Karger AG (Switzerland), 1991.

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11

Ellis, Jason A., i E. Sander Connolly. Vascular Biology of Cerebral Ischemia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0107.

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Carotid stenosis may be treated by carotid endarterectomy (CEA) or carotid artery stenting (CAS). Moderate asymptomatic carotid stenosis (50%-70%) is associated with a low risk of ischemic stroke and does not warrant treatment. The severe stenosis (>70%) population sees a marginal benefit in seen with CEA. In the Asymptomatic Carotid Atherosclerosis Study, authors concluded that for patients with less than 60% stenosis, a 5.9% absolute risk reduction was obtained over 5 years with CEA compared with maximum medical management (11 vs. 5.1%).

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12

Xiong, Xiaoxing, Heng Zhao, Creed Stary i Lijuan Gu, red. Immune Response to Cerebral Ischemia: Exploring Mechanisms and Potential Treatment Targets. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-326-1.

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13

N, Cohen Stanley, red. Management of ischemic stroke. New York: McGraw-Hill, Health Professions Division, 2000.

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14

Hypothermia and cerebral ischemia: Mechanisms and clinical applications. Totowa, NJ: Humana Press, 2003.

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15

(Editor), Carolina M. Maier, i Gary K. Steinberg (Editor), red. Hypothermia and Cerebral Ischemia: Mechanisms and Clinical Applications. Humana Press, 2003.

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16

M, Maier Carolina, i Steinberg Gary K, red. Hypothermia and cerebral ischemia: Mechanisms and clinical applications. Totowa, N.J: Humana Press, 2004.

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17

M, Maier Carolina, i Steinberg Gary K, red. Hypothermia and cerebral ischemia: Mechanisms and clinical applications. Totowa, N.J: Humana Press, 2004.

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18

R, Caplan Louis, red. Cerebrovascular ischaemia investigation and management. London: Med-Orion, 1996.

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19

Nicolaides, Andrew N., Wesley S. Moore, Louis R. Caplan i Edward G. Shifrin. Cerebrovascular Ischaemia: Investigation and Management. Med-Orion Publishing Co Ltd, 1996.

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20

(Editor), Sean I. Savitz, i Daniel M. Rosenbaum (Editor), red. Stroke Recovery with Cellular Therapies (Current Clinical Neurology). Humana Press, 2007.

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21

Rosenbaum, Daniel M., i Sean I. Savitz. Stroke Recovery with Cellular Therapies. Springer London, Limited, 2008.

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22

(Editor), James T. Robertson, i Thaddeus S., Jr. Nowak (Editor), red. Frontiers in Cerebrovascular Disease: Mechanisms, Diagnosis & Treatment. Futura Publishing Company, 1998.

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23

Hardy, Cheryl-Ann. The behavioral and physiological consequences of right middle cerebral artery ligation in rats following treatment with nimodipine, a calcium voltage-operated channel blocker. 1985.

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24

A, Ratcheson Robert, i Wirth Fremont P, red. Ruptured cerebral aneurysms: Perioperative management. Baltimore, MD: Williams & Wilkins, 1994.

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25

Acute ischemic stroke: An evidence-based approach. Hoboken, NJ: Wiley-Liss, 2007.

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26

Acute ischemic stroke: An evidence-based approach. Hoboken, N.J: John Wiley & Sons, 2008.

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27

Acute Ischemic Stroke: An Evidence-based Approach. Wiley-Liss, 2007.

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28

J, Reulen H., Philippon Jacques i European Association of Neurosurgical Societies. Meeting, red. Prevention and treatment of delayed ischaemic dysfunction in patients with subarachnoid haemorrhage: An update. Wien: Springer-Verlag, 1988.

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29

Ratcheson, Robert A., i Fremont P. Wirth. Ruptured Cerebral Aneurysms : Perioperative Management (Concepts in Neurosurgery, Vol. 6) (Concepts in Neurosurgery ; V. 6). Williams & Wilkins, 1994.

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30

Kevin Luk, K. H., i Deepak Sharma. Subarachnoid Hemorrhage. Redaktorzy David E. Traul i Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0024.

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Subarachnoid hemorrhage (SAH) is commonly caused by rupture of an intracranial aneurysm, arteriovenous malformation, or due to trauma. Prompt diagnosis and intervention are required to control intracranial pressure, maintain cerebral perfusion, and prevent rebleeding. Clinical grading of the bleed predicts morbidity and mortality, whereas imaging grading predicts risk of cerebral vasospasm. Hydrocephalus can occur as a result of SAH, which requires treatment with an external ventricular drain. Endovascular and open microsurgical procedures are available for securing the vascular abnormalities. Patients are typically monitored in a neurocritical care unit for up to 21 days post-bleed to monitor for the development of cerebral vasospasm/delayed cerebral ischemia (DCI). Mainstay of treatment for DCI includes induced hypertension, balloon angioplasty, and intraarterial vasodilator therapy. In addition, patient may experience significant derangement in their cardiac, pulmonary, and endocrine systems, requiring inotropic support, mechanical ventilation, or insulin infusion therapy.

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31

Gijn, Jan van. Stroke: A History of Ideas. Cambridge University Press, 2023.

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32

Stroke: Practical Mangement. Wyd. 3. Wiley-Blackwell, 2008.

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33

Mayor, Diana, i Michael Tymianski. Neuroprotection for Acute Ischemic Stroke. Redaktorzy David L. Reich, Stephan Mayer i Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0010.

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Acute ischemic stroke (AIS) is the leading cause of acquired neurological disability worldwide. AIS most commonly occurs when a cerebral artery is occluded, leading to irreversible brain injury and neurologic disability. Acute supportive physiological interventions and close monitoring on a stroke unit are beneficial to optimize overall recovery and functional outcome. Phamacological treatment options are limited though as the only FDA-approved therapy for AIS is the thrombolytic agent intravenous recombinant tissue plasminogen activator (Alteplase, rtPA), which improves functional outcome in therapeutic time windows ranging up to 3–4.5 hours. Several clinical trials assessing the efficacy of endovascular therapy have shown a benefit in carefully selected patients with a documented large vessel occlusion (LVO), and subsequently are becoming part of the standard practice in this AIS subset. Clinical trials using various imaging paradigms to enhance patient selection for thrombolytic therapy, endovascular therapy and neuroprotection therapies are all progressing.

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34

O’Neal, M. Angela. Postpartum Thunderclap Headache. Redaktor Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0018.

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An illustrative case of reversible cerebral vasoconstriction syndrome (RCVS) is presented. The clinical and radiographic features are reviewed. There is an overlap between RCVS and posterior reversible encephalopathy syndrome due to their shared pathophysiology related to endothelial injury. Furthermore, preeclampsia/eclampsia (PEE) is often associated with RCVS. Thunderclap headache is the most characteristic feature of the disorder. RCVS may also cause subarachnoid hemorrhage, typically located over the cerebral convexities; intracranial hemorrhage; and ischemic stroke. The diagnosis is made by seeing vasoconstriction on vessel imaging, either magnetic resonance angiography or computerized tomography angiography. There are several medications that can precipitate the condition by increasing sympathetic activity. Treatment is similar to that of PEE, with antihypertensives and magnesium. Calcium channel blockers are helpful symptomatic therapy for the headache.

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