Disease relevance of Intracranial Thrombosis

• METHODS: During a 1-year period, sera from patients with cerebral thrombosis or transient ischemic attack without cardioembolism were investigated for antibodies against B burgdorferi [1].
• METHODS: The authors performed interposed graft bypass operations using small vessels for four patients with moyamoya disease, six patients with cerebral thrombosis, and one patient with aortitis syndrome [2].
• The 3,150 outpatients (mean age, 68.9 years) were being treated by general practitioners and neurologists in Barcelona, Spain. Cerebral embolism was diagnosed in 4.0%, cerebral thrombosis in 13.0%, transitory ischemic attack in 28.0%, and chronic cerebral ischemia in 55.0% [3].
• In order to find out the relationship between the cerebrovascular acetazolamide reactivity and platelet function in asymptomatic cerebral thrombosis, 10 cases of asymptomatic cerebral infarction and 10 age-matched control subjects were studied [4].
• Stroke is a manifestation of long-term atherosclerotic disease, and in this study, plasma SSAO activities were estimated in 42 patients with cerebral thrombosis and 26 patients with cerebral embolism, and compared to two control groups of 45 individuals in total [5].

Psychiatry related information on Intracranial Thrombosis

• METHODS: We prepared formalin-fixed, paraffin-embedded sections from 33 autopsied brains, consisting of 7 normal controls, 4 cases with cerebral thrombosis, 5 cases with cerebral embolism, 8 cases with multiple lacunar infarctions, and 9 cases with Binswanger disease [6].

High impact information on Intracranial Thrombosis

• Cerebral thrombosis, cerebral haemorrhage, and ABO blood-groups [7].
• Letter: Tranexamic acid and intracranial thrombosis [8].
• Protease nexin-2/amyloid beta-protein precursor limits cerebral thrombosis [9].
• We hypothesized that the potent inhibition of certain procoagulant proteinases by PN2/AbetaPP, coupled with its abundance in platelets and brain, indicate that it may function to regulate cerebral thrombosis [9].
• However, those studies were potentially flawed because the genotypes of tPA-/- and wild-type control mice were not entirely clear, and ischemic neuronal injury was evaluated in isolation of tPA effects on brain thrombosis [10].

Chemical compound and disease context of Intracranial Thrombosis

• Induction of cerebral thrombosis with phenytoin in rats [11].
• Platelet volume, aggregation, and adenosine triphosphate release in cerebral thrombosis [12].
• Pentoxifylline would appear to be useful in most types of cerebrovascular disease including transient ischaemic attacks, sequelae of cerebral thrombosis and haemorrhage, and chronic ischaemic disorders [13].
• Cerebral thrombosis associated with Amicar therapy [14].
• It also delayed He-Ne laser-induced cerebral thrombosis and increased significantly the plasma concentration of nitric oxide metabolites (NO2/NO3) [15].

Biological context of Intracranial Thrombosis

• We compared whole blood platelet aggregation, adenosine triphosphate release, platelet count, platelet crit (percentage volume of platelets), and mean platelet volume during the acute, subacute, and chronic periods of cerebral thrombosis in 22 patients with value in 29 controls [12].
• The low cerebrovascular acetazolamide reactivity is considered to be related to platelet activation in asymptomatic cerebral thrombosis [4].
• An elderly patient with evidence of atherosclerosis and uremic bleeding diathesis developed two foci of cerebral thrombosis immediately after an infusion of desmopressin (DDAVP) [16].
• Platelet aggregation induced by collagen is enhanced in patients with cerebral thrombosis [1], and platelet aggregates and activation products such as beta-thromboglobulin appear in the circulation, particularly during the acute phase [2] [17].
• Protein C deficiency associated with massive cerebral thrombosis following open heart surgery [18].

Anatomical context of Intracranial Thrombosis

• The high levels of thrombomodulin in the chronic-phase cerebral thrombosis group suggests the presence of continuous endothelial cell damage [19].
• Erythrocyte rheology in acute cerebral thrombosis. Effects of ABO blood groups [20].

Gene context of Intracranial Thrombosis

• We injected recombinant t-PA into rats with cerebral 125I-labeled blood clot emboli to evaluate the dissolutive effect of recombinant human single-chain t-PA (rt-PA; TD-2061) on such emboli and to examine the possibility of improving neurological damage in patients with cerebral thrombosis [21].
• The results suggests that circulating HGF is a reliable early marker of cerebral infarction, and that this new sensitive HGF assay may be useful for diagnosing cerebral thrombosis [22].
• Severe arterial cerebral thrombosis in a patient with protein S deficiency (moderately reduced total and markedly reduced free protein S): a family study [23].
• Variations of alpha 2-plasmin inhibitor, antithrombin III, plasminogen in the serum of patients of cerebral thrombosis infused with urokinase [24].
• A simple and reproducible cerebral thrombosis model in rats induced by a photochemical reaction and the effect of a plasminogen-plasminogen activator chimera in this model [25].

Analytical, diagnostic and therapeutic context of Intracranial Thrombosis

• Effect of argatroban, a selective thrombin inhibitor, on animal models of cerebral thrombosis [26].
• Argatroban is a synthetic direct thrombin inhibitor which has been used in Japan for three indications, namely, chronic arterial occlusion, acute cerebral thrombosis and hemodialysis in AT-deficient patients or in patients with decreased AT [27].

References