What is the diagnosis and treatment approach for a patient suspected of having cerebral venous thrombosis?

Diagnosis and Management of Cerebral Venous Thrombosis

Diagnostic Approach

For patients with suspected cerebral venous thrombosis, obtain MRI with MR venography as the first-line imaging study, as it provides superior visualization of both venous occlusion and parenchymal changes compared to CT. 1, 2, 3

Clinical Presentation to Recognize

• Headache is the most common symptom, typically diffuse and progressively worsening over days to weeks (not sudden like arterial stroke) 2, 3
• Seizures occur in approximately 40% of patients—significantly higher than arterial stroke 2, 3
• Altered mental status without obvious focal deficits, particularly with deep venous system involvement (bilateral thalamic involvement) 2, 3
• Subacute presentation is typical: only 37% present acutely, 56% subacutely, and 7% chronically 2, 3

High-Risk Populations

• Women under 50 years, especially those on oral contraceptives or pregnant/postpartum 2, 3, 4
• Patients with prothrombotic conditions (protein C/S deficiency, antithrombin III deficiency, factor V Leiden) 2, 3
• Recent infection, malignancy, or inflammatory conditions 2, 3

Imaging Strategy

Primary imaging:

• MRI with MR venography shows both venous occlusion and parenchymal changes with highest sensitivity 1, 2, 3
• Add gradient echo T2 susceptibility-weighted imaging to improve diagnostic accuracy 1, 3

Alternative in emergency settings:

• CT venography if MRI unavailable or contraindicated 1, 2, 3
• Provides good visualization of major venous sinuses with 95% sensitivity and 91% specificity 1

Non-contrast CT limitations:

• Abnormal in only 30% of cases 2, 3
• May show "empty delta" sign or hyperdense cortical vein/dural sinus in acute phase 1, 2
• Normal CT does not exclude CVT—proceed to CTV or MRV if clinical suspicion remains high 2, 3

Diagnostic Pitfalls to Avoid

• Anatomic variants (sinus atresia/hypoplasia, asymmetrical sinus drainage) can mimic thrombosis—49% have asymmetrical lateral sinuses, 20% have partial/complete absence of one lateral sinus 1, 3
• Flow gaps on TOF MRV are common artifacts that affect interpretation 1, 3
• Median 7-day delay from symptom onset to diagnosis is common due to variable presentation 2, 3
• CVT may be misdiagnosed as idiopathic intracranial hypertension when presenting with isolated headache and papilledema 2, 3

Treatment Approach

Immediate Anticoagulation

Start anticoagulation immediately upon diagnosis with either intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin, even in patients with hemorrhagic lesions related to CVT. 2, 3, 5

• Anticoagulation prevents thrombus propagation, increases recanalization, and reduces mortality and severe disability 3, 5
• Do not withhold anticoagulation due to intracranial hemorrhage if it occurred as a consequence of CVT 3, 5

Duration of Anticoagulation

• Transient reversible risk factors (pregnancy, infection): 3-6 months of oral anticoagulation 3
• Idiopathic CVT or mild thrombophilia: 6-12 months 3
• High-risk inherited thrombophilia or recurrent events: Consider indefinite (lifelong) anticoagulation 3

Management of Elevated Intracranial Pressure

Use antiedema measures only in patients with significant mass effect and neurological deterioration, not routinely:

• Elevate head of bed to 20-30 degrees to facilitate venous drainage 5
• Mannitol 0.25-0.5 g/kg IV over 20 minutes (maximum 2 g/kg) as temporizing measure 5
• Hypertonic saline for clinical signs of transtentorial herniation 5
• Modest hyperventilation (PCO2 30-35 mm Hg) in intubated patients—recognize this is temporary only 5
• Avoid nitroprusside and other cerebral vasodilators 5
• Restrict free water to avoid hypo-osmolar fluids that worsen edema 5

Dexamethasone Use

Consider dexamethasone 4-8 mg/day (oral or IV) only for patients with significant white matter edema causing mass effect and neurological deterioration. 5

• Do not use routinely in all CVT cases or asymptomatic patients without significant mass effect 5
• Taper as quickly as clinically possible to minimize side effects (hyperglycemia, infection risk, personality changes) 5
• Long-term use (>3 weeks) carries significant toxicity 5

Seizure Management

• Treat seizures aggressively with antiepileptic medications 3
• Consider prophylaxis after first seizure, particularly in patients with hemispheric lesions 6

Advanced Interventions for Severe Cases

For patients with neurological deterioration despite anticoagulation:

• Endovascular thrombolysis or thrombectomy may be considered 2, 3
• Decompressive hemicraniectomy is life-saving for severe hemispheric cerebral edema with impending herniation 2, 3, 5
• Suboccipital decompressive craniectomy for cerebellar swelling with direct brainstem compression 5
• External ventricular drain if hydrocephalus present (high-risk in anticoagulated patients) 5

Follow-Up Imaging

• CTV or MRV at 3-6 months to assess recanalization 3
• Early repeat imaging for persistent or evolving symptoms despite treatment 3

Special Consideration: Vaccine-Induced Immune Thrombotic Thrombocytopenia (VITT)

If CVT occurs with thrombocytopenia and recent vaccination history:

• Immediately give intravenous immunoglobulin 1 g/kg to remove anti-PF4 antibodies 1
• Use non-heparin anticoagulants (direct oral anticoagulants, fondaparinux, argatroban, or danaparoid) due to potential cross-reactivity with heparin-induced thrombocytopenia 1
• Check D-dimer, coagulation screen, Clauss fibrinogen, and anti-PF4 antibodies 1