PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “CEREBRAL EMBOLISM AND THROMBOSIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,045 records · Page 58Linked to original sources
PubMed1995

Cerebral microembolism in patients with Sneddon's syndrome.

BACKGROUND: The pathogenesis of Sneddon's syndrome is unclear. This study addresses the question whether cerebral thromboembolism may be involved in the pathogenesis of the neurologic complications of the disorder. The study consisted of 13 patients with Sneddon's syndrome defined by both generalized livedo reticularis and a history of one or more cerebrovascular ischemic events; none had clinical or Doppler ultrasonographic evidence of atherosclerosis. METHODS: Transcranial Doppler microembolic monitoring of the middle cerebral artery; blood screening for antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibodies). RESULTS: Five patients (38%) showed clinically silent microembolism at transcranial Doppler monitoring, with individual microembolic event rates of the middle cerebral artery between 2 per hour and 33 per hour. In this group, the time since the last ischemic symptom was significantly shorter than in the eight patients without microemboli. Antiphospholipid antibodies were detected in three patients (23%), all of whom belonged to the microemboli-positive group. CONCLUSIONS: These data suggest that the detectability of both clinically silent cerebral microembolism and antiphospholipid antibodies may provide paraclinical evidence of active disease in patients with Sneddon's syndrome. The results support the notion that an immune-mediated prothrombotic state facilitating the formation of arterial thrombi with subsequent cerebral embolization, and/or triggering in situ thrombosis of cerebral vessels, plays a pathogenetic role in the neurologic manifestations of this disorder.

Adult↗
PubMed2006

[Heparin-induced thrombocytopenia: implictions for cardiologist].

Heparin-induced thrombocytopenia (HIT) is one of the most life-threatening adverse effects of heparin administration. It is characterized by thrombocytopenia and may also be associated with venous or arterial thrombosis. HIT type 2 is caused by the binding of antibodies, most likely IgG, to a complex of heparin and platelet factor-4, these complexes IgG/PF4/heparin activate platelets causing the release of pro-thrombotic particles that promote thrombin generation. HIT and HIT-thrombosis are associated with high morbidity and mortality. Thrombotic events are most frequently venous and may manifest as pulmonary embolism or cerebral venous thrombosis. Arterial thrombosis leading to limb damage and amputation and to myocardial infarction or stroke may also occur. HIT is a clinical syndrome that requires clinical and laboratory findings to confirm the diagnosis. All forms of heparin treatment should be stopped once HIT is suspected and patients should be treated with an alternative anticoagulant to treat and prevent thrombotic complications. Available alternative anticoagulants include argatroban and lepirudin, a recombinant form of hirudin.

Acute Disease↗