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

Among anti-phospholipid antibodies (APA), anti-cardiolipin antibodies and lupus anticoagulants are associated with arterial and venous thrombo-embolic manifestations. Antiphospholipid antibodies can be secondary to numerous diseases, especially systemic diseases, but they are usually encountered in the primary antiphospholipid syndrome. Neurological manifestations associated with APA are most often, if not always, ischemic in nature: large or small subcortical, often multiple, infarcts and transient ischemic attacks are the usual clinical presentations. Several mechanisms can lead to cerebral ischemia in the primary antiphospholipid syndrome, and their diagnosis is probably important for therapeutic choices. A prospective controlled study has started, which should provide data on the prognosis and management of this syndrome.
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PMID:[Antiphospholipid antibodies and the central nervous system]. 130 54

In a 2-year prospective study of 146 patients with cerebral ischemia, we compared vascular risk factors for stroke with clinical and laboratory findings, particularly antiphospholipid antibodies. Ten patients (6.8%) were positive for at least one antiphospholipid antibody; one patient had systemic lupus erythematosus, one had rheumatoid arthritis, and the remaining eight fulfilled criteria for the diagnosis of primary antiphospholipid syndrome. These patients were predominantly male, not necessarily young, and 50% of them did not have any other vascular risk factors; there were no significant clinical or paraclinical differences between these patients and those without antiphospholipid antibodies. Outcome in the 10 patients was good, and platelet antiaggregating drugs proved to be useful in preventing further cerebrovascular ischemic events in our patients.
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PMID:Antiphospholipid antibodies in cerebral ischemia. 205 74

One of the clinical hallmarks of antiphospholipid syndrome is the development of neurological complications, namely cerebral ischaemia, chorea, multi-infarct dementia, amaurosis fugax, migraine and transverse myelitis. An animal model should include the development of measurable neurological deficits and evidence of cerebral infarction. Although there are a number of mouse models for fetal loss, there has been no convincing model for the neurological complications of the antiphospholipid syndrome. One explanation for the high frequency of neurological events in antiphospholipid syndrome is a vulnerability of the cerebral vasculature to the hypercoagulable state associated with the syndrome. A greater appreciation of the differences in the regulation of coagulation between the systemic and cerebral vasculatures may be key to understanding the apparent predilection for central nervous system involvement in the antiphospholipid syndrome.
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PMID:Models for central nervous system complications of antiphospholipid syndrome. 780 11

We report clinical, neuroimaging and immunological findings in seven women with antiphospholipid antibodies (APLA) and cerebral ischemia. Two patients had systemic lupus erythematosus (SLE) and five had the antiphospholipid syndrome (APS). Autopsies were done in 3 women who died acutely with focal neurological deficits. Evidence for cerebral embolism was found in all patients: a) pathology demonstrated multiple cerebral infarctions and cerebral emboli from underlying non-bacterial thrombotic endocarditis (NBTE) in the patients who died. b) Three patients had thickened mitral valves and embolic cerebral occlusions were identified with cerebral angiography. c) In one patient, echocardiography detected a thrombus on the posterior leaflet of a prolapsing mitral valve at the time of ictus. Our data provide further evidence to implicate valvular endothelium in the genesis of cerebral ischemia in some patients with APLA.
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PMID:Focal cerebral ischemia and antiphospholipid antibodies: a case for cardiac embolism. 789 61

We report three children with hemidystonia in whom anti-cardiolipin (aCL) antibodies were demonstrated. Systemic lupus erythematosus was excluded on the basis of both clinical and serological criteria, and the diagnosis of primary antiphospholipid syndrome (PAPS) was made. In two cases, aCL antibodies could be causally related to a presumed immune-mediated thrombotic event involving the basal ganglia as shown by magnetic resonance imaging (MRI). In the remaining patient the finding of white matter alteration on NMR might be due to cross-reactivity of anti-phospholipid (aPL) antibodies with cerebral phospholipids, resulting in demyelination. We suggest that PAPS must always be considered when isolated or recurrent focal cerebral ischaemia, and particularly hemidystonia, occur in childhood.
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PMID:Hemidystonia symptomatic of primary antiphospholipid syndrome in childhood. 834 9

Antiphospholipid antibodies (aPL) have been associated with a variety of neurological disorders, mostly linked to focal neuroparenchymal ischemia or infarction. Cerebral ischemia associated with the antiphospholipid syndrome (APS) occurs at a younger age than typical atherothrombotic cerebrovascular disease, is often recurrent, and high positive GPL values are usually linked to the presence of a lupus anticoagulant. When other features of the syndrome are not present and cerebral ischemia occurs only associated with anticardiolipin immunoreactivity, there appears to be no discerning features of these patients unless GPL > 40 for which recurrent thrombo-occlusive events appear to occur more frequently. Other neurological manifestations associated with aPL include cerebral venous sinus thrombosis, ocular ischemia, dementia, including ischemic encephalopathy, and chorea. The role of aPL in migrainous events is controversial and may not play a role in recent, large case-controlled studies. Most seizures in patients harboring aPL are associated with focal brain infarction.
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PMID:Neurological aspects of antiphospholipid antibody syndrome. 890 59

Cerebral ischemia and infarction, intracerebral hemorrhage, subarachnoid hemorrhage, cerebral venous thrombosis, and cerebral vasculitis are dreaded but largely uncommon complications of most rheumatic diseases. In some conditions, however, such as the antiphospholipid syndrome or Behcet's disease, stroke may be the presenting complaint. A format for approaching the patient and localizing the cerebrovascular lesion has been presented along with a summary of the specific rheumatologic diseases implicated for each stroke subtype.
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PMID:Cerebrovascular complications of rheumatic disease. 915 94

The antiphospholipid antibody syndrome is characterized by the association between recurrent arterial or venous thrombosis and the presence of circulating antiphospholipid antibodies. Antiphospholipid antibody-related thrombosis seems to constitute a significant proportion of childhood thromboses. About one third of children suffering a thrombotic event have circulating antiphospholipid antibodies, and more than two thirds of children with idiopathic cerebral ischemia meet the criteria for the diagnosis of antiphospholipid antibody syndrome. Because the other risk factors for thrombosis commonly found in adults have no impact on the pediatric patient, the risk for thrombosis and thrombotic recurrences and the optimal anticoagulation therapy may differ from adults.
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PMID:Antiphospholipid antibody syndrome in pediatric patients. 928 81

The antiphospholipid syndrome, initially described in systemic lupus erythematosus (SLE), occurs in 20-35% of patients with this condition. Its clinical manifestations may precede, be concurrent with, or follow clinical features of SLE. There are no major differences between the primary antiphospholipid syndrome and the secondary form that associates with SLE. Several studies suggest that the presence of an antiphospholipid syndrome in patients with SLE conveys a worse prognosis. To prevent recurrence of thrombotic events (particularly arterial events), oral anticoagulation with an international normalized ratio (INR) close to 3 is recommended. Treatment of recurrent fetal loss is with aspirin, or with aspirin plus heparin. Controlled studies are underway to determine optimal treatment in patients with cerebral ischaemia as well as the optimal treatment in women with recurrent pregnancy loss.
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PMID:Antiphospholipid syndrome in SLE. 989 Jan 8

Echocardiographic studies have demonstrated a high prevalence of valvular disease in patients with primary antiphospholipid syndrome (PAPS). However, there are no studies assessing changes over time in valvular abnormalities. We conducted a study to determine whether there are changes over time in valvular lesions as detected by serial transesophageal echocardiography (TEE). Twelve patients with a first TEE had a second evaluation after a mean period of 13.5 months. There were 10 women and two men with a mean age of 38 years. Two patients had normal TEE on both initial and follow-up studies. Ten patients (83%) had valvular abnormalities, predominantly of the mitral and aortic valves in both studies. Abnormalities consisted of thickening, nodules, regurgitation, regurgitation and stenosis, and calcification. The type and frequency of lesions changed over time. As an example, one mitral valve nodule disappeared on follow up but three new aortic nodules developed even though all patients were receiving anticoagulant therapy. Two patients with mitral and aortic nodules presented cerebral ischemia. Mitral valvuloplasty was performed in one case. These results show that valvular abnormalities in patients with PAPS resolve, appear, or persist irrespective of anticoagulant therapy. Regurgitation is often mild or moderate, but stenosis may appear.
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PMID:[Valvulopathy in primary antiphospholipid syndrome. Prospective echocardiography study]. 1072 93


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