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Cerebral embolism

Zivin JA, Fisher M, DeGirolami U, Hemenway CC, Stashak JA. Tissue plasminogen activator reduces neurological damage after cerebral embolism. Science. 1985 230 1289-1292. [Pg.56]

Phillips DA, Fisher M, Smith TW, Davis MA. The safety and angiographic efficacy of tissue plasminogen activator in a cerebral embolization model. Ann Neurol. 1988 23 391-394. [Pg.56]

Cerebral Embolism Study Group. Immediate anticoagulation of embolic stroke a randomized trial. Cerebral Embolism Study Group. Stroke 1983 14 668-676. [Pg.160]

Cardiogenic brain embolism cerebral embolism task force. Arc/iAeurol 1986 43 71-84. [Pg.160]

Cardiogenic brain embolism. The second report of the cerebral embolism task force. Arch Neurol 1989 46 727-743. [Pg.210]

Ezura, M., Takahashi, A. and Yoshimoto, T. Evaluation of regional cerebral blood flow using single photon emission tomography for the selection of patients for local fibrinolytic therapy of acute cerebral embolism. Neurosurg. Rev. 19 231-236, 1996. [Pg.960]

AF or atrial flutter may be manifested by the entire range of symptoms associated with other supraventricular tachycardias, but syncope is not a common presenting symptom. An additional complication of AF is arterial embolization resulting from atrial stasis and poorly adherent mural thrombi, which accounts for the most devastating complication embolic stroke. Patients with AF and concurrent mitral stenosis or severe systolic HF are at particularly high risk for cerebral embolism. [Pg.75]

Thrombophlebitis, pulmonary or cerebral embolism, and retinal thrombosis occur rarely. [Pg.466]

Unlabeled Uses Prevention of myocardial infarction, recurrent cerebral embolism treatment adjunct in transient ischemic attacks... [Pg.1307]

More than 50% of patients with cerebral embolism have atrial fibrillation. In the majority of these patients, the underlying cardiac disease is nonvalvular. The risk of ischemic stroke and atrial fibrillation increases with age, reaching a cumulative risk of 35% during a patient s lifetime. Combined results from several randomized trials show that warfarin reduces the risk of stroke in patients with nonrheumatic atrial fibrillation by 68% (to 1.4% per year), with an excess incidence of major hemorrhage (including intracranial) of only 0.3% per year. [Pg.412]

Pearson TC, Wetherley-Mein G (1978). Vascular occlusive episodes and venous hematocrit in primary proliferative polycythemia. Lancet ii 1219-1222 Powers WJ (1986). Should lumbar puncture be part of the routine evaluation of patients with cerebral ischemia Stroke 17 332-333 Prior AL, Wilson LA, Gosling RG et al. (1979). Retrograde cerebral embolism. Lancet ii 1044-1047... [Pg.88]

Markus HS, Droste DW, Brown MM (1994). Detection of asymptomatic cerebral embolic signals with Doppler ultrasound. Lancet 343 1011-1012... [Pg.170]

Markus HS, Thomson ND, Brown MM (1995). Asymptomatic cerebral embolic signals in symptomatic and asymptomatic carotid artery disease. Brain 118 1005-1011... [Pg.301]

MacKinnon AD, Aaslid R, Markus HS (2005). Ambulatory transcranial Doppler cerebral embolic signal detection in symptomatic and asymptomatic carotid stenosis. Stroke 36 1726-1730... [Pg.328]

Ischemic strokes account for around 80-85% of all strokes and are caused by arterial vascular occlusions rarely occlusion in the cerebral venous system may result in ischemic and/or hemorrhagic stroke. Arterial occlusions resulting from cerebral embolism are the most common causes of ischemic strokes, and by about one week after stroke as many as 70-90% of occlusions will have spontaneously recanalized. Emboli typically originate from atherosclerotic stenoses in the internal carotid artery or from sources in the heart such as clots in the left atrium or the left ventricle. Hypertension-induced vascular disease of the small perforating intracerebral arteries is a common cause of lacunar strokes. A classification of the major stroke subtypes is shown in Table 31.1. [Pg.431]

Penry JK, Cordell AR, Johnston FR, and Netsky MG. Cerebral embolism by antifoam A in a bubble oxygenator system An experimental and clinical study. Surgery 1960 47 784-794. [Pg.689]

The main use of the coumarins is in the treatment and prevention of thromboembolic disease, including deep vein thrombosis, pulmonary embolism, and cerebral embolism from cardiac and other sources. [Pg.983]

Bowes, M. P., Zivin, J. A., and Rothlein, R., Monoclonal antibody to the ICAM-1 adhesion site reduces neurological damage in a rabbit cerebral embolism stroke model, Exp. Neurol., 119, 215, 1993. [Pg.72]

Such a cerebral thrombosis is believed to occur as a result of atherosclerotic damage in the arterial wall. Narrowing of the arterial lumen slows the blood flow. The projection of rough-surfaced deposits into what is by then a trickle of blood may serve as a nucleus around which the thrombus will form, thereby completing the occlusion. A variation is the wandering of a blood clot, or embolus, through the vasculature until finally it becomes wedged in a cerebral artery. This is a cerebral embolism. [Pg.422]

Streptokinase is contraindicated in patients with nlcerative wounds, active internal bleeding, recent trauma with possible internal injuries, visceral or intracranial malignancy, ulcerative cohtis, diverticulitis, severe hypertension, acute or chronic hepatic or renal insufficiency, uncontrolled hypoco-agnlation, chronic pulmonary disease with cavitation, sub-acnte bacterial endocarditis or rheumatic valvular disease, recent cerebral embolism, thrombosis, or hemorrhage, and diabetic hemorrhagic retinopathy, becanse excessive bleeding may occur. [Pg.652]

Calandie, L., J.F. Ortega, and E Bermejo, Anticoagulation and hemorrhagic infarction in cerebral embolism secondary to rheumatic heart disease. Arch Neurol, 1984. 41(11) p. 1152-4. [Pg.171]

Hewes RC, Auster M, White Rl (1985) Cerebral embolism first manifestation of pulmonary arteriovenous malformations in patients with hereditary hemorrhagic telangiectasia. CardioVasc Intervent Radiol 8 151-155... [Pg.294]

The doses for the procedure during interventional radiology are generally very high, e.g., 7.5-57 mSv for PTCA (percutaneous transluminal coronary angioplasty), 2-40 mSv for TIPS (transjugular intrahepatic portosystemic shunt), 17-25 mSv for radiofrequncy ablation, 5.7-20 mSv for cerebral embolization, and 0.3-24 mSv for biliary procedure (O Table 55.20). [Pg.2535]

There is a great variety of different coils currently available. Stainless steel coils have been used for a long time for peripheral embolizations. Due to an attached Dacron fibre they are extremely thrombo-genic, facilitating even parent vessel occlusion. They might be increasingly used for this indication, if detachable balloons are really not available any more. However, for cerebral embolizations they are too stiff. Platinum coils are much softer than stainless steel coils. Meanwhile, there exist different types of CE marked detachable platinum coils provided... [Pg.217]

Morino Y, Hara K, Tanabe K, et al. (2000) Retrospective analysis of cerebral complications after coronary artery bypass grafting in elderly patients. Jpn Circ J 64 46-50 Omran H, Schmidt H, Hackenbroch M, et al. (2003) Silent and apparent cerebral embolism after retrograde catheterisation of the aortic valve in valvular stenosis a prospective, randomised study. Lancet 361 1241-1246 Pichler P, Loewe C, Roedler S, et al. (2008) Detection of high-grade stenoses with multi-detector-row computed tomography in heart transplant patients. J Heart Lung Transplant 27 310 316... [Pg.250]

Cereals, 1134, 1135, 1138-1140, 1149 Cerebral blood flow, 3703, 3706, 3721 Cerebral embolism, 3703 Cerebral flow, 2301... [Pg.4176]

There are various mechanisms involved in decrease in cerebral blood flow. Research studies suggested three major events including increase uptake of glucose or decrease tissue glucose content, leads to increase glucose utilization and cerebral embolism which have cumulative effects on the cerebral blood flow (Fig. 122.4). [Pg.4699]

Fig. 122.4 Ginkgolides in cerebral blood flow inhibits the glucose uptake, decrease glucose utilization, inhibit decrease in ATP contents and inhibits cerebral embolism... Fig. 122.4 Ginkgolides in cerebral blood flow inhibits the glucose uptake, decrease glucose utilization, inhibit decrease in ATP contents and inhibits cerebral embolism...
Nervous system The association between cerebral microbleeds and the risk of recurrent hemorrhagic stroke in patients who have taken warfarin after cerebral embolic strokes associated with atrial fibrillation has been studied in 87 patients [6. Microbleeds were more common in patients with intracerebral hemorrhage than in those with cerebral infarction (87% versus 39%) and there were more of them per patient (8.4 versus 2.1). The mean INR was higher in patients with intracerebral hemorrhage (2.2 versus 1.4), as was the frequency of... [Pg.707]


See other pages where Cerebral embolism is mentioned: [Pg.150]    [Pg.361]    [Pg.559]    [Pg.356]    [Pg.149]    [Pg.1862]    [Pg.3108]    [Pg.332]    [Pg.173]    [Pg.245]    [Pg.242]    [Pg.45]    [Pg.395]    [Pg.174]    [Pg.215]    [Pg.242]   
See also in sourсe #XX -- [ Pg.242 ]




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Cerebral

Cerebral arteriovenous malformations embolic materials

Cerebral embolic

Cerebral embolic

Cerebritis

Embolism

Embolization

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