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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study reports the correlation of the thrombin generation test and the plasma clot impedance test with clinical evidence of hypercoagulability. Thrombin generation is increased and the rate of change of plasma from a liquid to a gel (clot impedance) is increased in situations where the risk of thrombosis is increased. These situations include increasing clinical signs and/or symptoms of thromboembolism, positive lung scans, postoperative total hip replacement, patients over 40 years old, low serum antithrombin III, thrombocytosis, transient cerebral ischemia, and positive isotope venogram for thrombosis. The two tests failed to indicate a significant effect of antiplatelet drugs on the hypercoagulable state. This study shows that the thrombin generation and plasma clot impedance tests are practical, rapid and useful tests for the detection and monitoring of the hypercoagulable state.
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PMID:Evaluation of the in vitro detection of the hypercoagulable state using the thrombin generation test and plasma clot impedance test. 50 79

An overview is given over etiology and prognosis of cerebral ischemias until the age of 40. In a time period of 19 years, 168 patients were diagnosed with cerebral ischemia until the age of 40 (91 females, 77 males). The most frequent etiology is premature atherosclerosis in patients with vascular risk factors (up to 50%). Cardiogenic embolism is responsible for 1 to 34% of the cases: cardiac valve diseases and endocarditis being the most frequent sources. In 2 to 19% a vasculitis is diagnosed. While infectious arteritis is especially frequent in countries of the third world, immunovasculitides are common in Europe and the USA. Noninflammatory vasculopathies include spontaneous or traumatic dissection, fibromuscular dysplasia and vascular malformations. A migrainous stroke is especially frequent in female smokers with intake of oral contraceptives. During pregnancy both sinus thrombosis and arterial ischemia occur. Hematologic causes for ischemia are polycythemia, thrombocytosis and genetic diseases (sickle cell anemia, AT3-deficiency). Cerebral ischemia may occur in connection with the ingestion of ergot-derivates. The prognosis of cerebral ischemia in young adults is better than in older stroke-patients.
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PMID:[Cerebral ischemia in young adults]. 193 40

The investigation of elderly patients presenting with raised PCV values has been described. Suitable clinical and laboratory investigation enables the separation of those with a raised red cell mass (RCM) into three groups: primary proliferative polycythaemia (PPP), secondary polycythaemia and idiopathic erythrocytosis. Those patients with a raised PCV but normal RCM either have apparent polycythaemia (normal plasma volume) or relative polycythaemia (low plasma volume). PPP is a clonal disorder with a peak incidence in the elderly. It commonly presents with vascular occlusive symptoms/signs involving larger vessels, both arterial and venous. The microvasculature may also be involved, particularly when there is associated thrombocythaemia. Effective treatment is required to minimize the future vascular occlusive incidence and diminish the complication rate of surgery if it is ever required. Both the PCV and the platelet count, if elevated, should be adequately controlled. 32P is probably the simplest treatment and is very effective, but venesection and intermittent low-dose busulphan is equally satisfactory in the co-operative patient with good peripheral veins. Secondary polycythaemia may arise from a variety of causes, particularly from arterial hypoxaemia and renal lesions. Occasionally, more than one pathology is identified in the elderly patient. Lung disease is the most common cause of hypoxaemia. Venesection may be indicated in those patients with excessively raised PCV values. The term idiopathic erythrocytosis should only be used for patients who have been adequately investigated. These patients most commonly present with ischaemic or vascular occlusive symptoms/signs. Relative polycythaemia may be caused by fluid loss, but generally the origin of the low plasma volume is not established. Apparent polycythaemia may represent a physiological variant or a stage before the development of a definitely raised RCM. The management of idiopathic erythrocytosis, and relative and apparent polycythaemia, should initially involved removal of known risk factors if present (e.g. hypertension) with the addition of venesection in selected patients. Reactive thrombocytosis in the elderly is most commonly due to malignant disease of chronic infection. The high platelet count is usually asymptomatic, and antiplatelet therapy is rarely required. Primary thrombocythaemia (PT) is a clonal myeloproliferative disorder similar to PPP. The finding of splenomegaly, abnormal platelet morphology or function helps to separate PT from reactive thrombosis. PT most commonly presents with digital or transient cerebral ischaemia or haemorrhage.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Polycythaemia and thrombocythaemia in the elderly. 332 42

Only two of 19 patients with spontaneously evolving essential thrombocythemia remained asymptomatic in a 421 patient-month observation. The rest of the patients showed hemorrhagic diathesis (four patients), nonspecific neurological semiology (two patients), and occlusive vascular illness in cerebral, myocardic, arterial, and often multiple locations (total, 12 patients). Peripheral neuropathy was found in five of 10 patients studied. In this series the incidence of cerebral ischemia in the uncontrolled condition was 180 times higher than the epidemiologic expectancy in a population not affected by the disorder. Of 35 ischemic attacks, 22 occurred when the platelet count was more than than 1000 X 10(9)/l, 13 when the count ranged from 650 to 990 X 10(9)/l, and none occurred at counts of less than 650 X 10(9)/l. In contrast, therapeutic control of the thrombocytosis caused all complications to disappear. These findings point out the danger of the natural course of the illness and justify active therapy. At the same time they call into question some of the most commonly used criteria in the diagnosis of essential thrombocythemia.
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PMID:Controlled and uncontrolled thrombocytosis. Its clinical role in essential thrombocythemia. 334 78

Reversible complete cerebro-circulatory arrest was produced in normothermic, anesthetized cats for 1 h by clamping the innominate and subclavian arteries, followed by blood recirculation of the brain for 30 min to 4 h. Blood volume of tissue samples was measured by intravenous injection of 125I-albumin and the platelet number by labelling of autologous platelets with 51Cr. The number of platelets trapped in the tissue was determined by subtracting from the total platelet count of the tissue sample those contained in the streaming blood, calculated from the blood volume by 125I-albumin. In sham-operated animals, after recirculation of autologous 51Cr labelled platelets for 60 min, no platelets were entrapped in the brain vasculature and total platelet number and fibrinogen concentration in the venous blood did not change. In animals submitted to complete cerebral ischemia for 1 h the number of trapped platelets increased significantly in the whole brain after 30 min of recirculation, i.e. the period of maximal postischemic vasodilatation and hyperemia, and highest concentrations were found in the border zone with 270 +/- 60 x 10(4) platelets/g tissue and in the brainstem with 240 +/- 70 x 10(4) platelets/g tissue. Blood platelets and fibrinogen concentration in the venous blood decreased significantly from 288 +/- 37 x 10(6)/ml and 299 +/- 50 mg% to 186 +/- 25 x 10(6)/ml platelets and 112 +/- 22 mg+ of fibrinogen, respectively. Platelets were nearly completely washed out of the brain after 4 h of recirculation. The highest increase of platelets was found in the kidney, lung and liver after 30 min of recirculation, indicating that intravascular coagulation following prolonged cerebral ischemia affects the extracerebral organs more than the brain itself.
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PMID:Effect of intravascular platelet aggregation on blood recirculation following prolonged ischemia of the cat brain. 615 3

This article addresses contraceptive issues for teenagers; women in the perimenopausal, postpartum, and postabortion periods; women with hematological disorders (e.g., acquired hemolytic anemia); women suffering from migraine; women with diabetes; and women with epilepsy. Specifically, it discusses how women's contraceptive needs change as they age. For example, the ideal method for perimenopausal women, who generally do not want to risk pregnancy, is male or female sterilization. The article also informs the reader what methods are most appropriate at the different periods of one's life and for various conditions. For example, since teens tend to be sexually active, the double Dutch method--condom plus combined oral contraceptive (COC) is a good practice for them. The low-dose lipid-friendly COC provides good cycle control for teens. Women with transient cerebral ischemia-related focal membrane, crescendo migraine, and focal migraine occurring for the first time after using COCs and currently use ergotamine therapy should absolutely not use COCs. The article also has tables which are helpful for practitioners. Table 1 lists the criteria for prescribing a medical contraceptive to teens without parental knowledge and consent. Table 2 explains either what contraceptives are or are not safe and effective for women with hemolytic disorders. For example, the IUD is contraindicated for women with immune thrombocytopenia purpura and thrombocythemia. A sidebar provides the reader a clinical focus.
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PMID:Contraceptive dilemmas. 807 39

Polycythemia vera (PV) can produce cerebral infarction. The mechanisms proposed by most authors are hyperviscosity-related diminished cerebral blood flow and platelet function abnormalities. We present a 36-year-old woman whose initial clinical manifestation of PV consisted of cerebral ischemia due to a carotid thrombus, as well as occlusion of the middle cerebral artery and cortical branches of the anterior cerebral artery demonstrated by angiography. To our knowledge, this is the first published case of cerebral infarction in PV caused by a thrombus of an extracranial artery. Therefore, PV can produce ischemic stroke due to thrombosis not only in small distal arteries or arterioles but also in the carotid artery or main branches. Treatment of intraluminal thrombus in non-arteriosclerotic carotid artery is discussed. Myeloproliferative disorders, including PV, must be suspected in all stroke patients with an elevated platelet count, even in those who have potential causes of reactive thrombocytosis.
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PMID:[Carotid thrombus and cerebral infarction as the initial clinical manifestation of polycythemia vera]. 1589 49

The role of genetic mutations in cerebral ischemia is not completely understood. Among these genetic variations, Philadelphia-negative gain-of-function mutation in the janus kinase 2 (JAK2) protein leads to overexpression of the genes involved in cell growth and proliferation, and has been linked to development of hematological malignancies, specifically, myeloproliferative neoplasms (MPNs; essential thrombocythemia [ET], polycythemia vera [PV], and primary myelofibrosis). Overt ET and PV are known to induce a prothrombotic state that leads to development of vascular complications, including cerebral arterial or venous thrombosis. Thromboembolism can precede overt presentation of an MPN by 2-3 years. As such, for the selected cases of embolic stroke or cerebrovascular sinus thrombosis with otherwise undetermined source and persistent thrombocytosis or polycythemia, in the absence of a confirmed MPN diagnosis, screening for JAK2 mutation may be reasonable, as early diagnosis and appropriate treatment can influence outcome by preventing recurrent thrombotic events. In this article, we review the literature on the genetics, pathogenesis, clinical manifestations, and treatment of JAK2-associated thrombosis, and present 2 cases of JAK2-associated cerebral arterial infarction and cerebral and systemic venous thromboembolism with otherwise negative etiology workup for stroke.
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PMID:Implications of Janus Kinase 2 Mutation in Embolic Stroke of Unknown Source. 3005 70