(Stroke. 2000;31:543.)
© 2000 American Heart Association, Inc.
Letters to the Editor |
Stroke Unit, Department of Neurology, St Janshospitaal, Bruges, Belgium
To the Editor:
In addition to the article of Longstreth et al1 recently published in Stroke, we describe 2 cases of stroke due to cerebral venous thrombosis with the G20210A mutation as only risk factor.
After sequencing of the gene for human prothrombin (factor II) by Degen and Davie2 in 1987, a new mutation of prothrombin (G20210A) was described by Poort et al3 in 1996. It is a common mutation of this factor associated with an increased risk of venous (and possible arterial) thrombosis, as stated by Martinelli et al.4 The mutation can be detected by a polymerase chain reactionrestriction fragment length polymorphism (PCR-RFLP) method, as described by Poort.3 Our laboratory uses this method.
Recently, we saw 2 patients with a definite diagnosis of cerebral venous thrombosis. No other known risk factor for cerebral venous thrombosis could be found. The finding of the abnormal mutation (G20210A) of factor II gene (both patients had a heterozygous state for the mutation) suggested this as etiology.
Patient 1 was a 42-year-old employee and moderate smoker. In his early
thirties he had an arterial thrombectomy in a
peripheral artery. In his family only his father had
suffered a "stroke." He was admitted to our hospital with a first
epileptic seizure, focal in origin. There was a venous infarction in
the right frontal lobe. MR angiography (including venous phase) showed
a typical stop in the frontal superior sagittal sinus, with loss of
draining veins. None of the other tests associated with venous
hypercoagulability showed
Department of Neurology
Department of Medicine, Division of Dermatology, University of Washington, Harborview Medical Center, Seattle, Washington
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