Cerebral venous thrombosis (CVT) is a blood clot that obstructs the brain’s venous sinuses, which are channels that drain deoxygenated blood from the brain. This blockage impedes drainage, causing blood to back up. This can increase pressure inside the head, potentially leading to swelling and bleeding within the brain.
CVT is a rare form of stroke, distinct from more common arterial strokes that block arteries supplying blood to the brain. Unlike arterial strokes, CVT predominantly affects younger adults and children. The condition can develop gradually over days or weeks, or it can manifest suddenly. Timely treatment is important for better outcomes.
Underlying Causes and Risk Factors
The formation of a blood clot in the brain’s veins is linked to factors that can be categorized as either genetic or acquired. Genetic, or prothrombotic, conditions create a natural predisposition for blood to clot more easily. Examples include inherited disorders like Factor V Leiden mutation, prothrombin gene mutations, and deficiencies in natural anticoagulant proteins like protein C, protein S, and antithrombin.
Acquired risk factors are conditions that develop during a person’s lifetime. Hormonal changes are a significant contributor, with pregnancy, the postpartum period, and oral contraceptives all increasing the risk for women. CVT is about three times more common in women than in men, a difference that diminishes with age. Severe dehydration can also thicken the blood, making clots more likely to form.
Certain medical conditions and infections can also precipitate CVT. Head and neck infections like sinusitis or mastoiditis can spread and trigger clot formation in nearby venous sinuses. Systemic inflammatory diseases and some cancers are also associated with a higher risk. Less common mechanical factors include direct head trauma or recent neurosurgical procedures.
Recognizing the Symptoms
The presentation of CVT varies among individuals, depending on the clot’s location and how quickly it formed. The most frequently reported symptom is a headache, occurring in about 90% of cases. This headache is often severe, persistent, worsens over several days, and may feel different from previous headaches. For about a quarter of patients, a headache may be the only symptom.
Seizures are a common feature, affecting up to 40% of individuals with CVT, a much higher rate than in arterial strokes. Vision problems, such as blurred or double vision, are also frequently noted. The increased pressure within the skull can cause swelling of the optic nerve, a condition known as papilledema, which is visible during an eye examination.
In more severe instances, CVT can cause stroke-like symptoms. These may include muscle weakness or numbness on one side of the body, difficulty with speech or understanding language, and decreased alertness or fainting.
Diagnostic Process
Diagnosing CVT begins with a clinical evaluation of the patient’s symptoms and medical history. Because the symptoms can be nonspecific and overlap with other conditions, a high degree of suspicion is often required. Following this assessment, specialized medical imaging is necessary to visualize the brain’s veins and confirm a clot.
The primary non-invasive diagnostic tools are Magnetic Resonance Imaging (MRI) with a Magnetic Resonance Venogram (MRV). This combination is highly sensitive and can directly show the clot or lack of blood flow in the venous sinuses. An alternative is a Computed Tomography (CT) scan with a CT Venogram (CTV), which uses contrast dye to provide detailed images of the veins. A standard CT or MRI without venography may not be sufficient to detect the clot.
Doctors may also order blood tests to investigate underlying causes, such as genetic clotting disorders, infections, or inflammatory markers. A D-dimer blood test, which measures a substance released when a clot breaks down, can sometimes help rule out CVT in low-risk patients. The definitive diagnosis, however, relies on imaging from an MRV or CTV.
Medical Treatments for CVT
The primary treatment for CVT is anticoagulation therapy, also known as blood thinners. The objective is to prevent the existing clot from growing and to stop new clots from forming, which gives the body a chance to dissolve the clot over time. Treatment often starts in the hospital with a fast-acting injectable anticoagulant, such as heparin.
Once stable, patients are transitioned to an oral anticoagulant for long-term management, such as warfarin or a direct oral anticoagulant (DOAC). The duration of therapy lasts for at least three to six months but can be longer depending on the underlying cause and whether the risk factor is temporary or permanent.
In a small number of severe cases where anticoagulation is not effective enough, more invasive procedures may be considered. One procedure is endovascular thrombolysis, where a catheter delivers clot-dissolving medication directly to the site. Another option is a mechanical thrombectomy to physically remove the clot. These interventions are reserved for patients with significant neurological symptoms or those deteriorating despite anticoagulant therapy.
Managing specific symptoms is also part of the treatment plan. Headaches are managed with pain-relieving medications, and anti-seizure medications are prescribed if seizures have occurred. When the clot causes a significant increase in pressure inside the skull, medications or procedures to lower this pressure may be necessary.