title: Coagulation studies, factor V Leiden, and anticardiolipin antibodies in 40 cases of cerebral venous thrombosis.
abstract: OBJECTIVE
  Cerebral venous thrombosis (CVT) is an infrequent condition with a large variety of causes. However, in 20% to 35% of cases, no cause is found. We studied coagulation parameters, including activated protein C resistance associated with factor V gene mutation (factor V Leiden) and anticardiolipin antibodies, in a large series of patients with CVT with or without identified cause or risk factor.
  
  
  METHODS
  Forty patients (30 women and 10 men) aged 19 to 71 years (mean age, 36.2 years) with CVT diagnosed by angiography and/or MRI were studied 1 to 18 years after thrombosis. No known cause was found in 10 idiopathic cases. Coagulation studies included the following tests: fibrinogen, antithrombin, protein C, protein S, plasminogen, anticardiolipin antibodies, activated protein C resistance, and factor V Leiden.
  
  
  RESULTS
  Six cases of thrombophilia (15%) were found: 1 protein C deficiency, 1 protein S deficiency, and 4 activated protein C resistance with heterozygous factor V Leiden mutation (10%). Only 1 case (protein S deficiency) was found in the group of 10 patients with idiopathic CVT. In the other 5, there was another cause or risk factor. Three patients (8%) had increased anticardiolipin antibodies: 1 with systemic lupus and 2 with primary antiphospholipid syndrome; 2 of these 3 patients also had factor V Leiden mutation.
  
  
  CONCLUSIONS
  Although present in a number of CVT cases, acquired (anticardiolipin) or congenital varieties of thrombophilia (factor V Leiden being the most frequent) are almost invariably associated with other predisposing factors. This suggests that (1) these abnormalities should be looked for in patients with CVT, whether a cause is found or not, and (2) their presence should not deter the search for other potential causes. The detection of such abnormalities has major practical consequences on the long-term management of patients to prevent further thrombotic episodes.
authors.affiliation: Service de Neurologie Hôpital Saint-Antoine, Paris, France.
authors.forename: M A
authors.initials: MA
authors.lastname: Deschiens
authors.forename: J
authors.initials: J
authors.lastname: Conard
authors.forename: M H
authors.initials: MH
authors.lastname: Horellou
authors.forename: A
authors.initials: A
authors.lastname: Ameri
authors.forename: M
authors.initials: M
authors.lastname: Preter
authors.forename: F
authors.initials: F
authors.lastname: Chedru
authors.forename: M M
authors.initials: MM
authors.lastname: Samama
authors.forename: M G
authors.initials: MG
authors.lastname: Bousser
mesh_terms: D000328:Adult; D000368:Aged; D017153:Antibodies, Anticardiolipin / Q000032:analysis*; D001777:Blood Coagulation; D001780:Blood Coagulation Tests; D002550:Cerebral Veins; D004351:Drug Resistance; D005165:Factor V / Q000235:genetics*; D005260:Female; D006579:Heterozygote; D006801:Humans; D002542:Intracranial Embolism and Thrombosis / Q000097:blood* / Q000235:genetics* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009154:Mutation; D011486:Protein C / Q000502:physiology; D020151:Protein C Deficiency; D018455:Protein S Deficiency / Q000150:complications
chemical_list: D017153:Antibodies, Anticardiolipin; D011486:Protein C; C095381:factor V Leiden; D005165:Factor V