Epidemiology And Risk Factors

In that no prospective, population-based, epidemiologic studies have been conducted to specifically examine CVT, the current incidence in the general population is not known. Most studies are from autopsy series (7-13). However, in the last decade an increase in diagnosis and survival of patients with CVT can be attributed to improved knowledge of hypercoagu-lable states, better detection via magnetic resonance imaging (MRI), which includes magnetic resonance venography (MRV), (Fig. 1) and increased use of intravenous anticoagulation as treatment. The ratio of CVT to arterial stroke is approximately 1 : 62.5 but only 1 : 8.5 in patients aged 15 to 45. CVT is more common in children (7 in 1,000,000/yr) than in adults (3 to 4 in 1,000,000/yr) and is reported in 7 out of 100,000 hospitalized adults (14,15).

Table 1 contains a list of risk factors for CVT. Approximately 75% to 85% of adult patients with CVT are women (2). The frequency of CVT was equal among men and women until the 1970s, when the widespread use of oral contraceptive (OC) pills came into use (2). Currently,

Figure 1 Magnetic resonance venography (MRV). Currently, many cerebral venous thromboses can be diagnosed noninvasively with the use of MRI and MRV, obviating the need to perform invasive catheter angiography.

75% of female cases present with CVT during pregnancy, during puerperium, or while they are taking OC pills. The prevalence of CVT associated with pregnancy or pueperium ranges from 2 to 500 per 100,000 deliveries, depending upon the country (1). During the last trimester and first 2 weeks postpartum, the risk of CVT is increased (16,17). Hormonal changes in males using androgens might also increase the risk of CVT. In 85% of people with CVT, a cause or prothrombotic risk factor can be identified.

Hypercoaguable states can be either inherited or acquired. Deficiencies of protein C, protein S, and antithrombin III can be inherited as autosomal-dominant conditions or acquired via inflammatory states, liver disease, disseminated intravascular coagulation, L-asparaginase therapy, and vitamin K deficiency. Deficiency of one of these anticoagulants is found in 2% to 12% of CVT patients (15,18,19). Activated protein C resistance can be inherited or acquired and is most commonly caused by factor V Leiden mutation (20). Factor V Leiden and prothrombin G20210A mutations are the most common inherited hypercoagulable states associated with CVT (10-20% of CVT patients) (15). Women who take OCs and who have genetic hypercoaguable predisposition, (e.g., factor V Leiden or prothrombin gene mutation) have an increased risk of developing CVT, compared to women of the same age who do not take OCs and do not have the factor V defect (21). An increased risk of CVT has also been reported in pregnant or puerper al women with factor V Leiden or prothrombin gene mutations (21). Abnormal recombinant plasminogen activator inhibitor-1 or lipoprotein(a) might also contribute to CVT because of decreased fibrinolysis. Prolonged elevation of clotting factors, such as fibrinogen and factor VIII, can increase the risk of venous thrombosis (22 ). Additionally, hyperhomocysteinemia and antiphospholipid antibodies, such as lupus anticoagulant and anticardiolipin antibodies,

Table 1 Risk Factors, Predisposing Conditions, and Causes of Cerebral Venous Thrombosis

Genetic hypercoagulable states Factor V Leiden mutation Antithrombin deficiency Protein C and protein S deficiency Prothrombin 20210A mutation

Hyperhomocysteinemia (gene mutations in methylenetetrahydrofolate reductase), homocystinuria Plasminogen deficiency Thrombomodulin gene mutation Sickle cell anemia and traits Hereditary dysfibrinogenemia P-Thalassemia Acquired prothrombotic states/hematologic conditions Thrombocythemia (primary or secondary) Nephrotic syndrome Antiphospholipid antibodies Hyperhomocysteinemia Pregnancy Puerperium

Increased resistance to activated protein C Paroxysmal nocturnal hemoglobinuria Leukemia, cancer

Anemia (posthemorrhagic, iron deficiency, hemolytic) Polycythemia

Heparin- or heparinoid-induced thrombocytopenia Disseminated intravascular coagulation Cryofibrinogenemia Elevated coagulation factors VII, VIII Protein C and protein S deficiency Infections Otitis, mastoiditis, sinusitis Meningitis

Systemic infectious disease (parasitic, fungal, viral, bacterial) Intracranial infection

(Continued)

Table 1 Risk Factors, Predisposing Conditions, and Causes of Cerebral Venous Thrombosis (Continued)

Inflammatory disease Systemic lupus erythematosus Wegener's granulomatosis Sarcoidosis

Inflammatory bowel disease (Crohn's disease, ulcerative colitis) Temporal arteritis Sjogren's syndrome Behcet's disease Drugs Oral contraception L-Asparaginase e-Aminocaproic acid Tamoxifen Epoetin alfa Lithium

Androgen therapy "Ectasy" Thyrotoxicosis Mechanical causes, trauma Head injury

Injury to sinuses of jugular vein, jugular catheterization Neurosurgical procedures Dural puncture Lumbar puncture Electrical injury Any surgical procedure Miscellaneous Dehydration, especially in children Dural arteriovenous malformations Tumors

Arachnoid cysts Congenital heart disease Congestive heart failure Pacemaker Carcinoid syndrome Cirrhosis

Ovarian hyperstimulation syndrome Severe exfoliative dermatitis have been detected in patients with CVT from 27% to 40% and 8% to 53%, respectively (15). Antiphospholipid antibodies are the most commonly acquired type of thrombophilia, although the mechanism in this setting remains unknown. Direct causes of sinus thrombosis include head injury or manipulation of the vasculature from neurosurgical procedures (i.e., catheterizations). Additionally, lumbar puncture can sometimes cause CVT from traction and deformation of the vessels.

Infections were the leading cause of CVT until the development of antibiotics. Otitis and mastoiditis can cause thrombosis via direct seeding to the adjacent sigmoid and transverse sinuses (Table 1 ).

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