Cerebral Venous Thrombosis
Cerebral venous thrombosis (CVT) is caused by thrombosis of the dural venous sinuses, cerebral veins, or both. It accounts for 0.5–3% of all strokes and predominantly affects younger individuals (<55 years), with two-thirds occurring in women. Unlike arterial stroke, CVT presents with diverse and often insidious symptoms—headache, seizures, focal deficits, and encephalopathy—that can mimic many other conditions, requiring a high index of clinical suspicion.
Despite its potentially devastating presentation, CVT carries a favorable prognosis overall: 80–90% of patients achieve functional independence (mRS 0–2). However, death or dependence still occurs in 10–15%, and chronic symptoms (headache, fatigue, cognitive impairment) affect quality of life in many survivors. Management centers on anticoagulation, with emerging evidence supporting direct oral anticoagulants (DOACs) as alternatives to vitamin K antagonists.
Bottom Line
- Presentation: Headache (~90%), seizures (20–40%), focal deficits (20–50%), and encephalopathy (up to 20%); symptoms often develop over days to weeks rather than acutely
- Diagnosis: MRI with MRV is the preferred modality (sensitivity 0.82, specificity 0.92); CT with CTV is a reasonable alternative; GRE/SWI sequences approach 100% sensitivity for cortical vein thrombosis
- Anticoagulation: LMWH is preferred acutely (even with intracranial hemorrhage), followed by transition to oral anticoagulation (VKA or DOAC) for 3–12 months depending on etiology
- DOACs: RE-SPECT CVT and ACTION-CVT support DOACs as safe and effective alternatives to warfarin; apixaban is the most commonly used (67% of DOAC-treated patients)
- Endovascular therapy: TO-ACT found no benefit over standard anticoagulation; reserved as rescue therapy for progressive deterioration despite adequate anticoagulation
Epidemiology and Risk Factors
CVT has an estimated incidence of 10–20 per million adults per year. In neonates, the incidence is substantially higher (6.4 per 100,000). Key demographic features include:
- Age: Predominantly affects individuals <55 years; median age ~40 years
- Sex: Two-thirds occur in women, largely driven by sex-specific risk factors (oral contraceptives, pregnancy)
- Geography: Higher reported incidence in low- and middle-income countries, possibly reflecting different risk factor profiles
Predisposing Factors
Predisposing factors are identified in the majority of patients and may be transient, chronic, or both. Many patients have >1 predisposing condition.
| Category | Transient | Chronic |
|---|---|---|
| Hormonal | Oral contraceptives (54–71%), pregnancy/postpartum (11–59%), HRT (4%) | Hormone replacement therapy, transgender hormonal treatment |
| Infection/Illness | Head/neck infections (8–11%), dehydration (2–19%), sepsis, COVID-19 (7.6%) | Obesity (23%), anemia (9–27%), thyroid disease, IBD (1–2%) |
| Medications | Corticosteroids, L-asparaginase, thalidomide, tamoxifen | — |
| Malignancy | — | Myeloproliferative disorders (2–3%), solid tumors (7%) |
| Autoimmune | — | Antiphospholipid syndrome (6–17%), SLE, Behçet disease, sarcoidosis (1%) |
| Genetic thrombophilia | — | Factor V Leiden, prothrombin G20210A, MTHFR C677T, protein C/S deficiency, antithrombin deficiency, JAK2 mutations (31–41% combined) |
| Mechanical | Head trauma (1–3%), neurosurgery, jugular catheterization (1–2%) | Meningioma compressing venous sinus, dural AV fistula |
Clinical Pearl: Oral Contraceptives and CVT
- Oral contraceptive use increases CVT risk nearly 8-fold
- Risk is synergistic with obesity and genetic thrombophilia
- Estrogen-containing formulations carry the highest risk
- Women with prior CVT should avoid combined hormonal contraceptives; progestin-only or non-hormonal methods are preferred
Clinical Presentation
The clinical presentation of CVT is highly variable, reflecting the location and extent of venous occlusion, the degree of venous congestion, and the presence of parenchymal injury. Symptoms tend to develop more insidiously than in arterial stroke—the majority present >48 hours after symptom onset.
Common Presentations
| Symptom | Frequency | Mechanism |
|---|---|---|
| Headache | ~90% | Raised intracranial pressure; may mimic migraine, thunderclap, or tension-type |
| Seizures | 20–40% | Cortical irritation from venous congestion or hemorrhagic infarction |
| Focal neurological deficits | 20–50% | Venous infarction; may not conform to arterial territories |
| Papilledema | 13–27% | Raised intracranial pressure from impaired CSF absorption |
| Visual disturbances | 13–27% | Transient visual obscurations, diplopia (CN VI palsy from raised ICP) |
| Encephalopathy/coma | Up to 20% | Extensive bilateral involvement, deep venous system thrombosis, or diffuse edema |
Syndromic Patterns
- Isolated intracranial hypertension: Headache with papilledema, visual obscurations, and CN VI palsy; no focal deficits or seizures. Most common with transverse/sigmoid sinus thrombosis.
- Focal syndrome: Focal deficits ± seizures, with or without headache. Mimics arterial stroke but deficits often do not respect arterial territories.
- Encephalopathy: Diffuse cerebral dysfunction with altered consciousness. Suggests extensive or bilateral involvement, particularly deep venous system.
- Thunderclap headache: Acute onset mimicking SAH; occurs in <5% but requires urgent evaluation.
Red Flags for CVT
- New or worsening headache in a young woman on oral contraceptives or peripartum
- Seizures with headache in the absence of a structural lesion
- Stroke-like deficits that do not conform to arterial territories
- Bilateral hemispheric involvement (hemorrhagic or edematous)
- Hemorrhagic infarction in a non-typical location (parasagittal, temporal)
- Progressive headache with papilledema
- Headache with new-onset seizure in a patient with thrombophilia or recent infection
Anatomy and Sinus Distribution
CVT can involve any of the dural sinuses or cortical/deep cerebral veins. Multiple sinuses are involved in 18–50% of cases.
| Venous Structure | Frequency | Clinical Correlates |
|---|---|---|
| Transverse sinus | 25–60% | Most commonly affected; often presents with isolated intracranial hypertension |
| Superior sagittal sinus | 25–45% | Bilateral parasagittal edema/hemorrhage; motor deficits; seizures |
| Straight sinus | 15–18% | Deep venous drainage; thalamic involvement; encephalopathy |
| Cortical veins | 15–17% | Focal cortical deficits, seizures; may be missed on routine CTV/MRV |
| Deep venous system | ~10% | Bilateral thalamic involvement; coma; worst prognosis |
| Sigmoid sinus | 5–15% | Often co-occurs with transverse sinus thrombosis |
| Internal jugular vein | ~10% | Concomitant with CVT, not in isolation |
Diagnostic Imaging
A high index of suspicion is essential because initial brain imaging (CT or MRI) may appear normal or show only indirect signs. Confirmatory venous imaging is required.
Initial Brain Imaging
Non-contrast CT is often the first test obtained. Direct signs of thrombus include:
- Cord sign: Hyperdense serpiginous or linear structure within a vein or sinus
- Dense triangle sign: Hyperdensity within the superior sagittal sinus (present up to 14 days)
- Cashew nut sign: Juxtacortical C-shaped hyperdensity (high specificity, low sensitivity)
Indirect signs include non-arterial territory edema, bilateral hemispheric hemorrhages, and hemorrhagic transformation within areas of venous congestion (present in up to 40%).
MRI is more sensitive than CT for detecting parenchymal lesions (venous infarctions, edema). Thrombus signal intensity varies with age:
- Acute (0–5 days): Isointense on T1, hypointense on T2 (deoxyhemoglobin)—can mimic flow void
- Subacute (5–15 days): Hyperintense on T1 and T2 (methemoglobin)—most easily recognized
- Chronic (>15 days): Variable signal; may be isointense on T2, mimicking flow
Imaging Tip: GRE/SWI for Cortical Vein Thrombosis
- Gradient-recalled echo (GRE) and susceptibility-weighted imaging (SWI) sequences have sensitivity approaching 100% for cortical vein thrombosis
- Thrombosed blood creates a blooming artifact on these sequences
- Standard CTV and time-of-flight MRV may miss isolated cortical vein thrombosis
- Always include GRE/SWI when CVT is suspected, even if the sinuses appear patent
Confirmatory Venous Imaging
| Modality | Sensitivity | Specificity | Key Features |
|---|---|---|---|
| CT venography (CTV) | 0.79 (0.76–0.82) | 0.90 (0.89–0.91) | "Empty delta sign" (filling defect in SSS); widely available; fast; lower sensitivity for cortical veins |
| MRI (conventional) | 0.82 (0.78–0.85) | 0.92 (0.91–0.94) | Preferred for parenchymal assessment; thrombus signal varies with age |
| MR venography (MRV) | High | High | TOF (no contrast) or contrast-enhanced; CE-MRV comparable to CTV; TOF susceptible to slow-flow artifacts |
| GRE/SWI | ~100% | High | Best for cortical vein thrombosis; blooming artifact from thrombosed blood |
| Digital subtraction angiography | Reference standard | Reference standard | Reserved for equivocal cases or when endovascular intervention is planned |
Recommended approach: MRI with T2*/SWI plus MRV is the preferred noninvasive study. CT with CTV is a reasonable alternative, particularly in centers with limited MRI access or when pretest probability is low.
D-dimer
D-dimer has limited diagnostic utility in CVT. It may be normal in patients with isolated headache, chronic CVT, or limited sinus involvement. A negative D-dimer does not exclude CVT and should not be used to defer imaging when clinical suspicion is present.
Etiological Workup
Once CVT is confirmed, a systematic evaluation for predisposing factors should be performed:
- Clinical evaluation: Assess for otitis, mastoiditis, facial/dental infection, dehydration, head trauma, stigmata of Behçet disease, malignancy, rheumatological conditions
- Exposures: Oral contraceptives, hormone therapy, chemotherapeutic agents, recent COVID-19 vaccination
- Laboratory tests: CBC, metabolic panel, coagulation studies (PT, aPTT), pregnancy test, D-dimer, ESR, iron studies
- Extended workup (as indicated): Hypercoagulation panel, antiphospholipid antibodies, JAK2 mutation, MTHFR, homocysteine, serum protein electrophoresis, COVID-19 testing
Thrombophilia Testing: When and What
- Not recommended routinely in all CVT patients
- Consider selectively in: young patients, spontaneous CVT without clear provoking factor, recurrent thrombosis, positive family history
- Acute-phase testing may yield false results—protein C, S, and antithrombin levels affected by acute thrombosis and anticoagulation
- If testing is needed, defer protein C/S and antithrombin measurement until after anticoagulation is completed
- Antiphospholipid antibodies and genetic tests (Factor V Leiden, prothrombin mutation) can be drawn acutely
Acute Management: Anticoagulation
Anticoagulation is the cornerstone of CVT treatment. The primary goals are to prevent thrombus propagation, facilitate recanalization, and prevent recurrent venous thromboembolism (VTE).
Initial Parenteral Anticoagulation
Both the AHA (2024) and European guidelines recommend initial treatment with subcutaneous low-molecular-weight heparin (LMWH), preferred over intravenous unfractionated heparin (UFH):
- LMWH is favored due to more predictable anticoagulation, lower risk of heparin-induced thrombocytopenia (HIT), and trends toward better outcomes in meta-analyses
- UFH is reserved for situations requiring rapid dose adjustment (impending surgery, severe renal impairment)
Intracranial Hemorrhage Is NOT a Contraindication
- Hemorrhagic transformation occurs in up to 40% of CVT patients at presentation
- The hemorrhage is a consequence of venous congestion, not a reason to withhold anticoagulation
- Anticoagulation treats the underlying cause (venous outflow obstruction) and prevents propagation
- Multiple studies confirm that anticoagulation does not worsen hemorrhage in CVT and may improve outcomes
Transition to Oral Anticoagulation
Once clinically and radiologically stable, transition from parenteral heparin to oral anticoagulation. Two options exist:
Vitamin K Antagonists (VKA)
- Traditional standard of care; target INR 2.0–3.0
- Transition after 5–15 days of lead-in heparin
- Required for patients with triple-positive antiphospholipid syndrome (DOACs are contraindicated)
- Required during pregnancy (use LMWH instead; both VKA and DOACs contraindicated)
Direct Oral Anticoagulants (DOACs)
Emerging evidence supports DOACs as safe and effective alternatives to VKA in CVT:
| Trial | Year | N | Design | Comparison | Key Findings |
|---|---|---|---|---|---|
| RE-SPECT CVT | 2019 | 120 | Prospective RCT | Dabigatran 150 mg BID vs warfarin (INR 2–3) | 0 recurrent VTE in either group; 1 major hemorrhage (dabigatran, GI) vs 2 (warfarin, ICH); no significant difference |
| SECRET | 2021 | 53 | Phase II RCT | Rivaroxaban 20 mg daily vs standard care (warfarin or LMWH) | 1 recurrent CVT + 1 sICH + 2 nonmajor bleeds in rivaroxaban; 0 VTE or bleeds in control; no safety concerns with early DOAC initiation (≤4 days lead-in) |
| ACTION-CVT | 2022 | 845 | Retrospective observational | DOAC vs VKA (real-world) | No significant difference in recurrent VTE (aHR 0.94); reduced major hemorrhage with DOACs (aHR 0.35, driven by lower ICH); apixaban 67%, rivaroxaban 18%, dabigatran 14% |
Practical Approach: Choosing Oral Anticoagulation
- Most patients: DOAC is a reasonable choice (apixaban most commonly used; rivaroxaban and dabigatran also supported)
- Triple-positive antiphospholipid syndrome: VKA required (DOACs associated with higher recurrent thromboembolism)
- Pregnancy/breastfeeding: LMWH only (DOACs and VKAs both contraindicated)
- Cancer-associated CVT: LMWH or DOAC; VKA less preferred
- Severe renal impairment: VKA preferred
- Lead-in parenteral anticoagulation for 5–15 days before transitioning to oral therapy is standard practice
Duration of Anticoagulation
The optimal duration depends on the underlying etiology and recurrence risk:
| Scenario | Recommended Duration | Rationale |
|---|---|---|
| Transient provoking factor (OCP, infection, dehydration, surgery) | 3–6 months | Low recurrence risk once provoking factor resolved |
| Unprovoked CVT (no clear etiology) | 6–12 months | Higher recurrence risk; longer treatment may reduce VTE recurrence |
| Severe thrombophilia (protein C/S deficiency, antithrombin deficiency, APS, combined defects) | Indefinite | High lifetime risk of recurrent VTE |
| Recurrent VTE (prior DVT/PE or recurrent CVT) | Indefinite | Demonstrated propensity for recurrence |
| Active malignancy | Duration of cancer treatment or indefinite | Ongoing prothrombotic state |
Recurrence Risk
The incidence of recurrent VTE after CVT ranges from 1–4% per year, with CVT-specific recurrence generally <1–2% per year. Risk factors for recurrence include:
- Severe thrombophilia (including malignancy)
- History of prior VTE
- Male sex (inconsistently reported)
- Absence of an identified precipitant
Endovascular Therapy
Endovascular treatment (EVT) options include intrasinus thrombolysis, mechanical thrombectomy, and combinations thereof. Despite theoretical appeal, evidence does not support routine use.
TO-ACT Trial
The TO-ACT trial (Thrombolysis or Anticoagulation for CVT) was a multicenter RCT that randomized 67 patients with severe CVT to EVT plus standard care versus standard care alone:
- mRS 0–1 at 12 months: 67% (EVT) vs 68% (control)—no difference (RR 0.99)
- Mortality: 12% (EVT) vs 3% (control)—numerically higher with EVT (not statistically significant)
- Trial stopped early for futility at interim analysis
Systematic reviews and meta-analyses have confirmed these findings: EVT is associated with higher mortality and no evidence of benefit in unselected populations.
When to Consider Endovascular Therapy
- EVT is currently reserved as rescue therapy for patients who are:
- Experiencing progressive neurological deterioration despite adequate anticoagulation
- Showing thrombus propagation on follow-up imaging despite treatment
- Having contraindications to anticoagulation
- Techniques include intrasinus thrombolysis (urokinase or rtPA), mechanical thrombectomy (stent retrievers, aspiration), and combined approaches
- No current evidence determines which EVT technique is superior
Decompressive Craniectomy
Decompressive craniectomy is a lifesaving intervention for patients with acute severe CVT and parenchymal lesions causing mass effect with impending herniation:
- Should be offered when there is midline shift, effacement of basal cisterns, or clinical signs of herniation
- Factors associated with poorer surgical outcomes: age >50, midline shift >10 mm, total effacement of basal cisterns
- A systematic review of 51 studies (483 patients) showed surgery within 48 hours may decrease mortality (OR 0.26; 95% CI 0.10–0.69) and improve functional outcomes
- No randomized controlled trials exist for this surgical approach
Seizure Management
Seizures are common in CVT (20–40% at presentation) and an important contributor to morbidity:
- Acute seizures: Treat with standard anti-seizure medications (levetiracetam is commonly used first-line)
- Prophylactic ASMs: Not routinely recommended; consider in patients with supratentorial hemorrhagic lesions or cortical involvement
- Epilepsy after CVT: Develops in >10% of patients; risk factors include seizures at onset, decreased consciousness, focal deficits, and hemorrhagic lesions
- Duration of ASM therapy: Individualized; patients without recurrent seizures may be weaned after 3–12 months
Special Populations
CVT in Pregnancy and Puerperium
Pregnancy and the puerperium account for 11–59% of CVT in women. The incidence ranges from 1 in 2,500 to 1 in 10,000 deliveries. Key considerations:
- Timing: Greatest risk during the third trimester and the first 6 postpartum weeks; ~80% of pregnancy-related CVT occurs after delivery
- Cesarean delivery: Associated with higher CVT risk (OR 3.10; 95% CI 2.26–4.24) after adjusting for other risk factors
- Prognosis: Generally equal to or better than non-pregnancy-related CVT
Management of CVT in Pregnancy
- Anticoagulation: Therapeutic-dose LMWH throughout pregnancy (DOACs and warfarin are contraindicated)
- Postpartum: LMWH or VKA (target INR 2.0–3.0) for minimum 6 weeks postpartum (total minimum 3 months)
- Breastfeeding: LMWH and warfarin are compatible; DOACs are contraindicated
- Future pregnancies: Not contraindicated, but prophylactic LMWH during future pregnancies and for 6 weeks postpartum is recommended
- Recurrence risk in future pregnancies: ~8 per 1,000 pregnancies (systematic review of 17 studies)
Pediatric CVT
CVT in children has a bimodal distribution: neonates (highest incidence, 6.4 per 100,000) and older children/adolescents. Key differences from adult CVT:
- Common precipitants: Sepsis (mastoiditis, Lemierre syndrome, COVID-19, meningitis), head trauma, hypoxia, dehydration, iron deficiency, sickle cell disease, nephrotic syndrome, cancer
- Presentation: May present with seizures, lethargy, poor feeding (neonates), or headache and focal deficits (older children); imaging typically requires anesthesia in young children
- Management: Parenteral anticoagulation (LMWH or UFH) in the acute phase
- Maintenance: LMWH, VKA, or rivaroxaban for at least 6 weeks (provoked VTE) to 3 months
- Mortality: ~3% in children; recurrent venous thrombosis ~6% (usually with no anticoagulation or lack of recanalization)
Key Pediatric Trials
| Trial | Year | N | Population | Key Finding |
|---|---|---|---|---|
| Kids-DOTT | 2023 | 417 | Age 4 months–20.9 years with provoked VTE (25% CVT) | 6 weeks of anticoagulation noninferior to 3 months for provoked VTE (including CVT) |
| EINSTEIN-Jr | 2023 | 114 | Children with confirmed CVT | Rivaroxaban: 0 recurrent VTE vs 1 in standard care; 5 nonmajor bleeds (rivaroxaban) vs 1 major subdural bleed (standard); recanalization rates similar |
Vaccine-Induced Immune Thrombocytopenia and Thrombosis (VITT)
VITT emerged in 2021 following adenoviral vector COVID-19 vaccination (AstraZeneca ChAdOx1, Janssen Ad26.COV2.S). CVT was the most common thrombotic manifestation. Key features:
- Timing: 5–24 days after vaccination; headache is the most common presenting symptom
- Mechanism: Antibodies to platelet factor 4 (PF4) that activate platelets, similar to autoimmune HIT
- Key lab finding: Thrombocytopenia + positive anti-PF4 antibodies (ELISA, not rapid assays)
- Incidence: Rare (estimated 4–16 per million first-dose adenoviral vector vaccines)
- Mortality: 39–61% in initial cohorts; improved with early recognition and appropriate treatment
- No association with mRNA vaccines (Pfizer BNT162b2, Moderna mRNA-1273)
VITT Management Protocol
- Avoid heparin (may worsen platelet activation, though evidence is uncertain)
- Nonheparin anticoagulants: Argatroban or fondaparinux first-line; transition to DOAC once platelets recover
- IVIG: 1 g/kg body weight daily for 2 days
- Steroids: Recommended adjunctive therapy
- Platelet transfusions: Not recommended (may fuel thrombosis)
- Multidisciplinary management: Hematology consultation essential
Prognosis and Long-Term Outcomes
Functional Outcomes
- 80–90% of patients achieve functional independence (mRS 0–2)
- Death or dependence in 10–15% despite treatment
- Early mortality (~30 days): ~3.4%, primarily from ICH with herniation (48%) and cancer (21%)
- One-year mortality: ~5.6%
Prognostic Factors for Poor Outcome
| Poor Prognostic Factor | Notes |
|---|---|
| Advanced age | Especially >50 years |
| Active cancer | Leading cause of late mortality; 3.9× higher VTE recurrence + hemorrhage |
| Decreased level of consciousness | GCS <9 at presentation |
| Intracerebral hemorrhage | Hemorrhagic lesions at baseline or during treatment |
| Deep venous system involvement | Straight sinus, internal cerebral veins, vein of Galen |
| Male sex | Inconsistently associated with worse outcomes |
| Bilateral involvement | Superior sagittal sinus involvement with bilateral edema/hemorrhage |
Chronic Symptoms
Despite achieving functional independence, many CVT survivors experience persistent symptoms that impact quality of life:
- Headache: Chronic headache is the most common residual complaint
- Cognitive impairment: Impaired concentration, processing speed, memory
- Fatigue: Significant and often underrecognized
- Mood disturbance: Depression and anxiety are common
- Return to work: In one study, 42% of working/student patients had not returned to work or school at 6 months despite 87% reaching functional independence
- Post-CVT epilepsy: Develops in >10% of patients
Management Algorithm
| Step | Action | Details |
|---|---|---|
| 1. Suspect CVT | Clinical assessment | Headache + risk factors (young woman, OCP, peripartum, thrombophilia, infection); seizures with non-arterial territory lesion |
| 2. Imaging | MRI + MRV (preferred) or CT + CTV | Include GRE/SWI sequences; evaluate for parenchymal hemorrhage, edema, mass effect |
| 3. Etiological workup | Identify predisposing factors | CBC, coagulation, pregnancy test, infection screen; selective thrombophilia panel |
| 4. Acute treatment | Parenteral anticoagulation | LMWH preferred (even with ICH); UFH if rapid reversal needed; treat seizures |
| 5. Stable: oral transition | VKA (INR 2–3) or DOAC | After 5–15 days of parenteral therapy; pregnancy: LMWH only; APS: VKA only |
| 5b. Progressing despite AC | Consider EVT or craniectomy | EVT for thrombus propagation; craniectomy for herniation with mass effect |
| 6. Duration | 3–12 months or indefinite | Based on etiology: transient (3–6 mo), unprovoked (6–12 mo), severe thrombophilia/recurrent VTE (indefinite) |
| 7. Follow-up | Clinical + imaging reassessment | CTV or MRV at 3–6 months to assess recanalization; evaluate for chronic symptoms; address modifiable risk factors |
Dural Arteriovenous Fistula After CVT
Dural arteriovenous fistula (dAVF) is a recognized complication of CVT, with a reported prevalence of 2.4% at a median follow-up of 8 months in one large retrospective series (n=1,218). The relationship is bidirectional—CVT can cause dAVF through neovascularization of the occluded sinus wall, and dAVF can predispose to CVT through altered venous hemodynamics. Follow-up venous imaging should be considered to evaluate for this complication.
References
- Saposnik G, Bushnell C, Coutinho JM, et al. Diagnosis and management of cerebral venous thrombosis: a scientific statement from the American Heart Association. Stroke. 2024;55:e77–e90.
- Ferro JM, Canhao P, Stam J, et al. Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). Stroke. 2004;35:664–670.
- Ferro JM, Bousser MG, Canhao P, et al. European Stroke Organization guideline for the diagnosis and treatment of cerebral venous thrombosis. Eur Stroke J. 2017;2:195–221.
- Yaghi S, Shu L, Bakradze E, et al. Direct oral anticoagulants versus warfarin in the treatment of cerebral venous thrombosis (ACTION-CVT): a multicenter international study. Stroke. 2022;53:728–738.
- Ferro JM, Coutinho JM, Dentali F, et al. Safety and efficacy of dabigatran etexilate vs dose-adjusted warfarin in patients with cerebral venous thrombosis (RE-SPECT CVT): a randomized clinical trial. JAMA Neurol. 2019;76:1457–1465.
- Coutinho JM, Zuurbier SM, Bousser MG, et al. Effect of endovascular treatment with medical management vs standard care on severe cerebral venous thrombosis: the TO-ACT randomized clinical trial. JAMA Neurol. 2020;77:966–973.
- Field TS, Weitz JI, Engbers JDT, et al. Study of Rivaroxaban for Cerebral Venous Thrombosis (SECRET): a phase II exploratory randomized controlled trial. Stroke. 2023;54:2724–2732.
- Monagle P, Newall F, Barnes C, et al. Kids-DOTT: a randomized trial evaluating 6 weeks vs 3 months of anticoagulation for pediatric venous thromboembolism. NEJM. 2023;389:2400–2410.
- Male C, Thom K, Engbers J, et al. EINSTEIN-Jr: oral rivaroxaban for pediatric cerebral venous thrombosis. Blood Adv. 2023;7:6254–6264.
- Bousser MG, Ferro JM. Cerebral venous thrombosis: an update. Lancet Neurol. 2007;6:162–170.
- Schulman S, Kearon C, Kakkar AK, et al. Dabigatran versus warfarin in the treatment of acute venous thromboembolism. NEJM. 2009;361:2342–2352.
- Coutinho JM, Ferro JM, Canhao P, et al. Cerebral venous and sinus thrombosis in women. Stroke. 2009;40:2356–2361.