Fatal Cerebral Venous Sinus Thrombosis Associated with the Factor V Leiden Mutation and the Use of Oral Contraceptives

1995 ◽  
Vol 74 (05) ◽  
pp. 1382-1382 ◽  
Author(s):  
Françoise Bridey ◽  
Michel Wolff ◽  
Jean Pierre Laissy ◽  
Véronique Morin ◽  
Martine Lefebvre ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Zeynep Ozcan Dag ◽  
Yuksel Işik ◽  
Yavuz Simsek ◽  
Ozlem Banu Tulmac ◽  
Demet Demiray

Preeclampsia is a leading cause of maternal mortality and morbidity worldwide. The neurological complications of preeclampsia and eclampsia are responsible for a major proportion of the morbidity and mortality for women and their infants alike. Hormonal changes during pregnancy and the puerperium carry an increased risk of venous thromboembolism including cerebral venous sinus thrombosis (CVST). Factor 5 leiden (FVL) is a procoagulant mutation associated primarily with venous thrombosis and pregnancy complications. We report a patient with FVL mutation who presented with CVST at 24th week of pregnancy and was diagnosed as HELLP syndrome at 34th week of pregnancy.


2007 ◽  
Vol 91 (2) ◽  
pp. 243-245 ◽  
Author(s):  
M Abrantes ◽  
AF Lacerda ◽  
CR Abreu ◽  
A Levy ◽  
A Azevedo ◽  
...  

1970 ◽  
Vol 10 (2) ◽  
pp. 115-118
Author(s):  
Naima Sultana ◽  
Monzurul H Chowdhury ◽  
Md Shahriar Mahbub ◽  
Md Billal Alam

Cerebral venous sinus thrombosis is a rare disorder accounting for less than 1% of all strokes. It is more common in children and young adults. Here we report a rare and interesting case of cerebral venous l sinus thrombosis mimicking subarachnoid hemorrhage. A 40 years old women, presented with sudden onset of headache, vomiting and unconsciousness associated with convulsions. She had a history of taking oral contraceptives for the last 12 years. Clinical examinations showed ill-looking women with Glasgow Coma Scale of 12 along with neck rigidity and bilateral papilloedema. Although initially we suspected her as a case of subarachnoid hemorrhage, subsequent investigations with MRI and MRV showed to be a case of superior sagittal and transverse sinus thrombosis. Treatment with anticoagulation recovered her from headache and papilloedema. Serum levels of thrombophilic factors were within the normal physiological limits. Thus we concluded that although cerebral venous thrombosis is 100 times less than the cerebral arterial disease, a women presented with sudden onset of headache and vomiting with long term use of oral contraceptives, cerebral thrombosis should be considered as a differential.  Key words: Cerebral venous sinus thrombosis , Sagittal sinus thrombosis, Subarachnoid hemorrhage , Magnetic resonance venography. doi: 10.3329/jom.v10i2.2826   J MEDICINE 2009; 10 : 115-118


2009 ◽  
Vol 27 (5) ◽  
pp. E5 ◽  
Author(s):  
Marcelo Galarza ◽  
Roberto Gazzeri

Object The goal of this study was to provide data about neurosurgical management of cerebral venous sinus thrombosis in young women after use of oral contraceptives. Methods Between 1990 and 2007, the authors treated 15 women (age range 23–45 years) in whom neurosurgical management was used for overt thrombosis of cerebral sinus. All were healthy, with a history of use of oral contraceptives. Severe headache was the most common symptom, followed by motor focal deficits and comatose state. Deep infarcts were located in the thalamic and basal ganglia region in 11 cases. Seven women had associated intracerebral hemorrhage, and 3 had ventricular dilation. Angiographic MR imaging was done in 10 patients, and conventional angiography was done in 7. Genetic analysis of chromosomal abnormalities associated with stroke was done in 5 cases. Results The intracranial pressure (ICP) was monitored in all cases. Three patients underwent external ventricular drainage, and 1 had a decompressive craniotomy. All had absence of signal in the cerebral sinus rectus, with associated thrombosis of the transverse sinus in 7 cases. Angiograms were negative for additional vascular malformation. Medical treatment included sodium heparin and mannitol in 9 cases, and enoxaparin in the other 6 patients. Genetic analysis was positive for prothrombin mutation G20210A (factor II variant) in 2 cases. The mean follow-up duration of 53 months demonstrated no neurological deficit in 10 patients, hemiparesis in 3, and severe hemiparesis with aphasia in 1 case. One woman died 5 days after a decompressive craniotomy. Conclusions Cerebral venous sinus thrombosis secondary to oral contraception in young women, including lesions in critical and deep regions, can be treated medically with acceptable morbidity. In spite of this, a subgroup of patients needed basic neurosurgical management of the lesions, including surgical measures for controlling raised ICP.


2019 ◽  
Vol 12 ◽  
pp. 175628641989515 ◽  
Author(s):  
Carmen Serna Candel ◽  
Victoria Hellstern ◽  
Tania Beitlich ◽  
Marta Aguilar Pérez ◽  
Hansjörg Bäzner ◽  
...  

A 34-year-old female patient presented during the 10th week of her second gravidity with headache, nausea and vomiting 2 weeks before admission. Her medical history was remarkable for a heterozygous factor V Leiden mutation, elevated lipoprotein A, and a cerebral venous thrombosis (CVT) after oral contraceptive intake 15 years before. Magnetic resonance imaging (MRI) suggested acute and massive intracranial sinus thrombosis. Despite full-dose anticoagulation, the patient deteriorated clinically and eventually became comatose. Now, MRI/magnetic resonance angiography revealed vasogenic edema of both thalami, of the left frontal lobe, and of the head of the caudate nucleus, with venous stasis and frontal petechial hemorrhage. She was referred for endovascular treatment. Diagnostic angiography confirmed a complete superficial and deep venous sinus occlusion. Endovascular access to the straight and superior sagittal sinus was possible, but neither rheolysis nor balloon angioplasty resulted in recanalization of the venous sinuses. Monitored heparinization was continued and antiaggregation was initiated. The patient remained comatose for another 5 days and MRI showed progress of the cytotoxic edema. On day 6, infusion of eptifibatide at body-weight-adapted dosage was started. The following day, the patient improved and slowly regained consciousness. MRI confirmed regression of the edema. The eptifibatide infusion was continued for a total of 14 days. Thereafter two doses of 180 mg ticagrelor per os (PO) daily were started. The patient remained on acetylsalicylic acid (ASA), ticagrelor, and enoxaparin on an unchanged dosage regimen. She was discharged home 26 days after the endovascular treatment without serious neurological deficit, with the pregnancy intact. At the 30th week of pregnancy the dosage of ASA was reduced to 300 mg once PO daily. Cesarian delivery was carried out at the 38th week of pregnancy. The newborn was completely healthy. Ultima ratio therapeutic options for severe intracranial venous sinus thrombosis refractory to anticoagulation are discussed, with an emphasis on platelet-function inhibition.


2021 ◽  
Vol 10 (34) ◽  
pp. 2960-2963
Author(s):  
Maria Prothasis ◽  
Yash Gupte ◽  
Sourya Acharya ◽  
Samarth Shukla ◽  
Neema Acharya

Thrombosis of cerebral venous channel is a known complication of hypercoagulable states. Hyperhomocysteinaemia is a known hypercoagulable state. Obesity is a modern-day global epidemic. Disorders such as myocardial infarction (MI), stroke, and venous thromboembolism are on the rising trend and its increased morbidity and mortality is being associated with obesity. To date, however, the knowledge about the association between obesity and adult cerebral venous thrombosis (CVT) is sparse. We report a 44-year-old young morbidly obese metabolically unhealthy female who presented with headache, nausea, vomiting and giddiness. On evaluation, magnetic resonance venogram showed cerebral venous sinus thrombosis. On investigations, she had concomitant hyperhomocysteinaemia and metabolic syndrome. Cerebral venous sinus thrombosis causing stroke in young adults is uncommon with various conditions precipitating it.1,2,3 Severe headache (70 - 90 %), focal lateralized signs (25 % - 75 %), seizures (30 – 40 %) as well as behavioural symptoms such as delirium, amnesia, and disturbances in consciousness are the various associated clinical symptoms. The known inherited hypercoagulable risk factors that cause CVST are gain of function mutations in the genes encoding factor V (factor V Leiden) and prothrombin, Protein C, S and antithrombin III deficiency. Hyperhomocysteinaemia, is a known risk factor for causing venous thrombosis of the lower limbs. However, till date there is no data available showing its role in causing cerebral venous thrombosis. The interaction between genetic and acquired determinants result in high plasma levels of total homocysteine (tHcy).4,5,6 Vitamins such as folic acid, pyridoxine, and cobalamin are involved in the metabolic pathways of homocysteine and its deficiencies represent the acquired determinants. Venous thromboembolism (VTE) comprises of deep vein thrombosis of the leg and pulmonary embolism and obesity is now being recognised as one of the risk factors causing it. The risk of VTE is approximately increased to 2-fold in an individual with a body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared) of 30 or more compared with a normal BMI (< 25), and higher BMIs increase more risk with approximately 3 times higher risk in individuals with a BMI greater than 40.7, 8,9 Again obesity as a risk factor for CVST is less known.


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