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Cerebral strokes

Cellular therapy is the replacement of unhealthy or damaged cells or tissues with new ones. Because neurodegenerative diseases, cerebral strokes and traumatic injuries to the CNS produce neurological deficits that result from neuronal loss, cell therapy is a major area of investigation for the treatment of neurological diseases and injuries. [Pg.96]

After cerebral stroke and traumatic brain injury, there is a striking amount of neurological recovery in the following months and years, despite often-permanent structural damage. The increase in neurogenesis would also be a factor contributing to the plasticity of CNS, particularly in relation to the recovery in the CNS after injury. [Pg.112]

Treatment of cerebral stroke patients with selective serotonin reuptake inhibitor antidepressant showed difference in improvement with respect to laterality. The post-stroke major depressive disorder improved much more in right stroke subjects in comparison with the left stroke ones (Spalletta el al., 2003). In case of unilateral brain injury due to stroke or parkinsonism, the intact hemisphere plays an important role in recovery and compensation for the lost motor function (Schallert el al., 2003). A well-selected homeopathic potency may facilitate recovery by acting on the intact hemisphere. It has been demonstrated that the brain can asymmetrically... [Pg.79]

Huisman TA (2003) Diffusion-weighted imaging basic concepts and application in cerebral stroke and head trauma. Eur Radiol 13 2283-2297... [Pg.129]

Hilal SK, Maudsley AA, Simon HE, Perman WH, Bonn J, Mawad ME, Silver AJ, Ganti SR, Sane P, Chien IC (1983) In vivo NMR imaging of tissue sodium in the intact cat before and after acute cerebral stroke. AJNR Am.J.Neuroradiol. 4 245-249... [Pg.181]

The early risk of stroke after TIA also depends on the vascular territory of the event. Monocular events are associated with a low risk of subsequent cerebral stroke (Hankey et al. 1991, Benavente et al. 2001). Posterior circulation TIAs, which make up approximately 25% of all attacks, were thought for many years to be associated with a lower risk of stroke than carotid territory TIAs (Sivenius et al. 1991 Mohr et al. 1992 Caplan 1996). Correspondingly, they were often managed less aggressively. [Pg.201]

Lovastatin is a member of a class of drugs (atorvastatin and simvastatin are others in this class) called statins that are used to treat hypercholesterolemia. The statins act as competitive inhibitors of the enzyme HMG-CoA reductase. These molecules mimic the structure of the normal substrate of the enzyme (HMG-CoA) and act as transition state analogues. While the statins are bound to the enzyme, HMG-CoA cannot be converted to mevalonic acid, thus inhibiting the whole cholesterol biosynthetic process. Recent studies indicate that there may be important secondary effects of statin therapy because some of the medical benefits of statins are too rapid to be a result of decreasing atherosclerotic lesions. Statin therapy has been associated with reduced risks of dementia, Alzheimer disease, ischemic cerebral stroke, and other diseases that are not correlated with high cholesterol levels. Although this is still an active area of research, it appears that the pleiotropic effects of statins may be a result of a reduction in the synthesis of isoprenoid intermediates that are formed in the pathway of cholesterol biosynthesis. [Pg.315]

Hypertension and atherosclerosis are central to the pathogenesis of coronary artery disease (ischemia, angina, myocardial infarction) heart failure, cerebral (stroke) and peripheral vascular disease. [Pg.88]

IIM-HAOI Inlcrnalional (.170-740) perfusion, cerebral stroke, ischemia. [Pg.414]

Murakami, T., Okamoto, K., Ogaki, M., and lizuka, Y. (1987). Effect of Chlorella on blood pressure, cerebral stroke lesions, hypertensive vascular change and life-span in spontaneously hypertensive rats. Nippon Eiyo Shokuryo Gakkaishi. 40,351-359. [Pg.322]

In those cases In which the cause of death could be studied (Table VI), we found a higher Incidence of renal and cardiovascular causes In the hypertensive than In the normotensive group, while cerebral strokes were alike. Four cases died because of complications of the renal transplant In patients with secondary renal gout. The other causes of death were diverse, being striking those due to the admIn I St rat Ion of drugs used to control the gout. [Pg.98]

Christopher, R., Nagaraja, D., and Shankar, S.K., 2007. Homocysteine and cerebral stroke in developing countries. Current Medical Chemistry. 14 2393-2401. [Pg.531]

Salonen JT, Puska P, Tuomilehto J. Physical activity and risk of myocardial infarction, cerebral stroke and death. Am J Epidemiol 1982 115 526-537. [Pg.97]

Technetium-99m exametazime [(RR,3 3)-4,8-diaza-3,6,6,9-tetramethylundecane-2,10-dionebisoxime] is used as an adjunct in the detection of altered regional cerebral perfusion in stroke. The kit for the preparation of the radiopharmaceutical is suppHed as a single dose vial. [Pg.484]

Stroke. A general term commonly used to denote a sudden paralysis resulting from a cerebral hemorrhage. [Pg.455]

Pignataro G, Gala R, Cuomo O et al (2004) Two sodium/ calcium exchanger gene products, NCX1 andNCX3, play a major role in the development of permanent focal cerebral ischemia. Stroke 35 2566-2570... [Pg.808]

PI (adenosine) receptors were explored as therapeutic targets before P2 receptors. Adenosine was identified early and is in current use to treat supraventricular tachycardia. A2a receptor antagonists are being investigated for the treatment of Parkinson s disease and patents have been lodged for the application of PI receptor subtype agonists and antagonists for myocardial ischaemia and reperfusion injury, cerebral ischaemia, stroke, intermittent claudication and renal insufficiency. [Pg.1052]

Prevention of a repeat cerebral thrombosis in some patients who have experienced a stroke ... [Pg.425]

FIGURE 2.6 Dynamic susceptibility contrast imaging. Axial images of the brain are acquired repeatedly, in this case every 1.5 seconds. As a bolus of intravenously injected contrast material enters the brain, first arteries, then brain parenchyma, and finally veins demonstrate a transient loss of signal intensity. In this acute stroke patient, hypoperfusion of the left middle cerebral artery territory results in delayed arrival of the contrast bolus and prolonged stasis of contrast within the tissue. [Pg.16]

Horowitz SH, Zito XL, Donnarumma R, Patel M, Alvir X. Computed tomographic-angiographic findings within the first five hours of cerebral infarction. Stroke 1991 22 1245-1253. [Pg.28]

Wardlaw JM, Dorman PJ, Lewis SC, Sandercock PAG. Can stroke physicians and neuroradiologists identify signs of early cerebral infarction on CT J Neurol Neurosurg Psychiatry 1999 67 651-653. [Pg.29]

Slivka A, Murphy E, Horrocks L. Cerebral edema after temporary and permanent middle cerebral artery occlusion in the rat. Stroke 1995 26 1061-1065. [Pg.32]

Hunter GJ, Hamberg LM, Ponzo JA, Huang-Hellinger FR, Morris PP, Rabinov J, Farkas J, Lev MH, Schaefer PW, Ogilvy CS, Schwamm LH, Buonanno FS, Koroshetz WJ, Wolf GL, Gonzalez RG. Assessment of cerebral perfusion and arterial anatomy in h3fperacute stroke with three-dimensional functional CT early clinical results. Am J Neuroradiol 1998 19 29-37. [Pg.32]

Lev MH, Segal AZ, Farkas J, Hossain ST, Putman C, Hunter GJ, Budzik R, Harris GJ, Buonanno FS, Ezzeddine MA, Chang Y, Koroshetz WJ, Gonzalez RG, Schwamm LH. Utility of perfusion-weighted CT imaging in acute middle cerebral artery stroke treated with intra-arterial thrombolysis prediction of final infarct volume and clinical outcome. Stroke 2001 32 2021-2028. [Pg.32]

Endo H, Inoue T, Ogasawara K, Fukuda T, Kanbara Y, Qgawa A. Quantitative assessment of cerebral hemodynamics using perfusion-weighted MRI in patients with major cerebral artery occlusive disease comparison with positron emission tomography. Stroke 2006 37 388-392. [Pg.33]

Sorensen AG, Copen WA, 0stergaard L, Buonanno FS, Gonzalez RG, Rordorf G, Rosen BR, Schwamm LH, Weisskoff RM, Koroshetz WJ. Hyperacute stroke simultaneous measurement of relative cerebral blood volume, relative cerebral blood flow, and mean tissue transit time. Radiology 1999 210 519-527. [Pg.34]

Parsons MW, Yang Q, Barber PA, Darby DG, Desmond PM, Gerraty RP, Tress BM, Davis SM. Perfusion magnetic resonance imaging maps in hyperacute stroke relative cerebral blood flow most accurately identifies tissue destined to infarct. Stroke 2001 32 1581-1587. [Pg.34]

Wintermark M, Reichhart M, Thiran JP, Maeder P, Chalaron M, Schnyder P, Bogous-slavsky J, MeuU R. Prognostic accuracy of cerebral blood flow measurement by perfusion computed tomography, at the time of emergency room admission, in acute stroke patients. Ann Neurol 2002 51 417-432. [Pg.36]

Ischemic stroke has numerous causes. Cerebral infarction may result from large artery atherosclerosis, cardiac embolism, small artery lipohyalinosis, cryptogenic embolism, or, more rarely, from other diverse conditions such as arterial dissection, infective endocarditis, and sickle cell disease. Arterial occlusion is the cause of at least 80% of acute cerebral infarctions. " ... [Pg.39]

Based primarily on the study protocol of the 1995 NINDS rt-PA study.Many centers would also exclude patients with known documented endocarditis or aortic dissection, and those with CT hypoattenuation in more than one third of the middle cerebral artery territory. There are insufficient data to support the use of rt-PA for ischemic stroke in pregnancy or in the pediatric population (age <18 years). [Pg.42]


See other pages where Cerebral strokes is mentioned: [Pg.19]    [Pg.111]    [Pg.79]    [Pg.53]    [Pg.414]    [Pg.74]    [Pg.19]    [Pg.111]    [Pg.79]    [Pg.53]    [Pg.414]    [Pg.74]    [Pg.130]    [Pg.189]    [Pg.200]    [Pg.201]    [Pg.608]    [Pg.181]    [Pg.2]    [Pg.8]    [Pg.12]    [Pg.12]    [Pg.13]    [Pg.33]    [Pg.37]    [Pg.44]   
See also in sourсe #XX -- [ Pg.19 , Pg.96 , Pg.111 ]




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Hemorrhage into cerebral stroke

Stroke cerebral blood flow

Stroke patients, cerebral blood

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