Disease relevance of Intracranial Embolism

• Fetal death did not occur in the 12 cases in which subcutaneous heparin was substituted for the coumarin derivative in the first trimester and the last 2 weeks of pregnancy (group III), but maternal cerebral embolism developed in 8.3% of the patients [1].
• Symptoms of embolism, the second frequent presentation in the classic triad, were observed in 33 cases (29%) with 1 or several locations, essentially cerebral emboli with stroke [2].
• We examined the relationship between free protein S deficiency and cerebrovascular disease by reviewing the records of all patients with the diagnoses of cerebral thrombosis, cerebral embolism, and cerebral vascular occlusion who were referred for coagulation studies over a 12-month period [3].
• CONCLUSIONS: Tirilazad pretreatment reduces neurologic deficits from multiple cerebral emboli [4].
• Indomethacin and cerebrovascular permeability to albumin in acute hypertension and cerebral embolism in the rat [5].

High impact information on Intracranial Embolism

• CONCLUSION: Cerebral protection with the GuardWire device is easy, safe, and effective in protecting the brain from cerebral embolism [6].
• METHODS: We intravenously administered recombinant tissue plasminogen activator (20-30 MU for 1 hour) to 10 patients with acute (less than 6 hours) brain embolism and examined the neurological outcomes in relation to the findings on computed tomography and angiography [7].
• Cholesterol cerebral emboli have been rarely reported as a cause of lacunes [8].
• Tuberous sclerosis with cardiogenic cerebral embolism: magnetic resonance imaging [9].
• Cerebral embolism as the initial manifestation of peripartum cardiomyopathy [10].

Chemical compound and disease context of Intracranial Embolism

• Effect of cerebrospinal fluid removal on cerebral blood flow and metabolism in the baboon: influence of tyrosine infusion and cerebral embolism on cerebrospinal fluid pressure autoregulation [11].
• Therapeutic efficacy of tirilazad in experimental multiple cerebral emboli: a randomized, controlled trial [4].
• 1. The present study was designed to determine whether naftidrofuryl oxalate exerts a possible therapeutic effect on brain energy metabolism impaired by microsphere-induced cerebral embolism in vitro [12].
• Naftidrofuryl oxalate improves impaired brain glucose metabolism after microsphere-induced cerebral embolism in rats [13].
• The succinate dehydrogenase activity of the brain mitochondria isolated from rats 3 days after the cerebral embolism was significantly decreased [14].

Biological context of Intracranial Embolism

• Tissue glucose and glycogen greatly increased after cerebral embolism, suggesting embolism-induced inhibition of glycolysis [13].
• We used an experimental multiple cerebral embolism model to test whether treatment with tirilazad (U74006F), a putative inhibitor of lipid peroxidation, would improve functional outcome after multiple brain emboli [4].

Anatomical context of Intracranial Embolism

• This significant protective effect suggests that pretreatment with tirilazad may play a role in clinical situations where the risk of cerebral emboli is high, with changes in leukocyte adherence as a potential mechanism [4].
• The present study was undertaken to elucidate pathophysiological changes in noradrenaline (NA) transporter and Na+/K+-ATPase, key regulators of cation gradient across the plasma membrane, in nerve terminals of the cerebral cortex after microsphere-induced cerebral embolism in rats [15].
• Therefore, we investigated alterations of tight junctional proteins, i.e., occludin and zonula occludens (ZO)-1, in isolated rat brain capillaries after microsphere-induced cerebral embolism [16].
• Recombinant t-PA (rt-PA) was labeled with technetium-99m (99mTc) to investigate the in vivo binding to fibrin clots in a feline cerebral embolism model created by insertion of an artificial fibrin clot within the carotid artery [17].

Gene context of Intracranial Embolism

• Fibrinolytic effect of tissue plasminogen activator on cerebral embolism in stroke-prone spontaneously hypertensive rats [18].
• To study the thrombolytic effect of tissue plasminogen activator (t-PA) on cerebral emboli, we characterized cerebral embolization in stroke-prone spontaneously hypertensive rats (SHRSPs) and Wistar Kyoto rats (WKYs) [18].
• Enzyme activities of hexokinase, phosphofructokinase and pyruvate kinase were not inhibited, but rather increased slightly after cerebral embolism [13].
• CONCLUSIONS: Silent cerebral embolism frequently occurs during transcatheter PFO and ASD closure [19].
• Cerebral embolism in a patient with polycythemia rubra vera [20].

Analytical, diagnostic and therapeutic context of Intracranial Embolism

• Asymptomatic circulating cerebral emboli and cerebral blood flow velocity under aspirin and ticlopidine in patients with cerebrovascular disease [21].
• Carotid tissue levels of argatroban after direct local delivery during carotid endarterectomy to prevent perioperative cerebral embolism [22].
• Transcranial Doppler ultrasonography was used to quantitate cerebral emboli and xenon-133 clearance was used to measure cerebral blood flow [23].
• CONCLUSION: In both CEA and CAS, recording of cerebral emboli by TCD ultrasonography provides insight in the pathogenesis of procedure related adverse cerebral outcome [24].
• Two-dimensional echocardiography revealed in the first case multiple masses of thrombi in the dilated ventricle consistent with congestive cardiomyopathy and emergency surgery was performed for cerebral embolism [25].

References