Cerebral thrombosis

The other serious side effects include high blood pressure, increased risk of myocardial infarction, thromboembolic diseases like thrombophlebitis, venous thrombosis, cerebral thrombosis. 

Contraindications History of thromboembohc disorders, deep venous thrombosis, cerebral vascular disease, myocardial infarction, liver cancer, estrogen-dependent cancer, breast cancer, undiagnosed abnormal genital bleeding, or suspected pregnancy. 

A condition in which there are excess macroglobulins in the blood. The high levels of large molecular weight proteins lead to sluggish blood flow and this, in turn, can result in thrombosis in the small blood vessels. Retinal vein thrombosis, cerebral thrombosis and peripheral gangrene (hyperviscosity syndrome) are features. 

Aspirin has been remarkably successful in the treatment of the pain and swelling of inflammatory disease and in fact, an estimated 45,000 tons of aspirin are still consumed each year. This success resulted in the syntheses of many other aspirin-like drugs , now referred to as NSAIDs. Aspirin, however, continues to have a unique use in the prevention of thrombosis. Since it produces irreversible inhibition of COX-1 by acetylation of serine at position 530 in the active site, a daily low dose of aspirin will cause a cumulative inhibition of COX-1 in platelets, in the portal circulation. A gradual inhibition of platelet aggregation occurs, reducing the possibility of occlusion of coronary or cerebral vessels by platelet thrombi. However, there are no systemic... 

Kleinschnitz C, Stoll G, Bendszus M et al (2006) Targeting coagulation Factor XII provides protection from pathological thrombosis in cerebral ischemia without interfering with hemostasis. J Exp Med 203 513-518... 

Prevention of a repeat cerebral thrombosis in some patients who have experienced a stroke ... 

This category includes patients with rare causes of strokes such as nonatherosclero-tic vasculopathies, cerebral venous thrombosis, hypercoagulable states, or hematologic disorders. Two such disorders are discussed below. 

Dissection of the internal carotid and vertebral arteries is a common cause of stroke, particularly in young patients. Although many occur due to trauma, it is estimated that over half occur spontaneously. The mechanism of stroke following arterial dissection is either by artery-to-artery embolism, by thrombosis in situ, or by dissection-induced lumenal stenosis with secondary cerebral hypoperfusion and low-flow watershed infarction. Occasionally, dissection may lead to the formation of a pseudoaneurysm as a source of thrombus formation. Vertebrobasilar dissections that extend intracranially have a higher risk of rupture leading to subarachnoid hemorrhage (SAH). ° ... 

Kalbag RM, Woolf AL. Cerebral venous thrombosis. London University Press 1967. 

Ameri A, Bousser M. Cerebral venous thrombosis. Neurol Clin 1992 10 87-111. 

Bousser MG. Cerebral venous thrombosis nothing, heparin, or local thrombolysis Stroke 1999 30 481 83. 

Frey JL, Muro GJ, McDougall CG, Dean BE, Jahnke HK. Cerebral venous thrombosis combined intrathrombus rtPA and intravenous heparin. Stroke 1999 30 489 94. 

Smith AG, Cornblath WT, Deveikis JP. Local thrombolytic therapy in deep cerebral venous thrombosis. Neurology 1997 48 1613-1619. 

Holder CA, Bell DA, Lundell AL, Ulmer JL, Glazier SS. Isolated straight sinus and deep cerebral venous thrombosis successful treatment with local infusion of urokinase. J Neurosurgery 1997 86 704-707. 

Monitor for evidence of cerebral edema, noncardiogenic (permeability) pulmonary edema, acute respiratory distress syndrome, hyperchloremic metabolic acidosis, and vascular thrombosis... 

Martinelli I, Sacchi E, Landi G, Taio-li E, Duca F, Mannucci PM. High risk of cerebral-vein thrombosis in carriers of a prothrombin-gene mutation and in users of oral contraceptives. N Engl J Med 1998 338[25] 1793-1797. 

Suggested Alternatives for Differential Diagnosis Meningitis, basilar artery blood clots (thrombosis), cardioembolic stroke, cavernous sinus syndromes, cerebral venous blood clots (thrombosis), confusional states and acute memory disorders, epileptic and epileptiform encephalopathies, febrile seizures, haemophilus meningitis, intracranial hemorrhage, leptomeningeal carcinomatosis, subdural pus (empyema), or bruise (hematoma). 

K+ channels K-atp Rat brain Diabetes, asthma, cardiac arrythmia, angina, cardiac and cerebral ischemia, thrombosis, hypertension, incontinence, pain, neurogenic inflammation, epilepsy, stroke, hair growth Control of insulin release, vasodilatation, protection against cell ischemia... 

Since the early 1980s, much effort has focused on animal models of acute and chronic neurodegeneration in search of therapeutics for stroke. Neuronal cell death follows strokes, acute ischemic insults, and chronic neurodegeneration, such as Parkinson s disease, Alzheimer s disease (AD), epilepsy, and Huntington s disease. Up to 80% of all strokes result from focal infarcts and ischemia in the middle cerebral artery (MCA), so the commonly used animal models for neuroprotection are produced by temporary or permanent occlusion of the MCA.5 Lesions of the MCA include occlusion by electrocoagulation, intraluminal monofilaments, photochemical effects, thrombosis, and endothelin-1, but all of these models necessitate studying reperfusion events and validating MCA occlusion by behavioral assessments. 

In a totally different field, studies were being carried out on children who had a deficiency of methionine synthase and an impaired ability to convert homocysteine to methionine, so that they had increased blood levels of homocysteine. It was noted that these children had an increased incidence of thrombosis in cerebral and coronary arteries. This led to a study which eventually showed that an increased level of homocysteine was a risk factor for coronary artery disease in adults. Since methionine synthase requires the vitamins, folic acid and B12, for its catalytic activity, it has been suggested that an increased intake of these vitamins could encourage the conversion of homocysteine to methionine and hence decrease the plasma level of homocysteine. This is particularly the case for the elderly who are undernourished (see Chapter 15 for a discussion of nutrition in the elderly). 

Unlabeled Uses Acute peripheral occlusive disease, basilar artery occlusion, cerebral infarction, deep vein thrombosis, femoropopliteal artery occlusion, mesenteric or subclavian vein occlusion, pleural effusion (parapneumonic)... 

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