Cerebral venous thrombosis (CVT) is a thrombotic obstruction of the cerebral venous system that can lead to ischemic lesions (or hemorrhages) in the brain. The condition can occur at any age and is often associated with a hypercoagulable state, a trigger (e.g., delivery, head injury, CNS instrumentation) or an infection (i.e., as in septic CVT). Women are affected more frequently than men, possibly as a result of the additional risk factors of pregnancy and oral contraceptive use. Cavernous sinus thrombosis is a rare subset of CVT that is most often due to infections in the paranasal region. Headache is the most common symptom of CVT and, depending on the size and location of the clot, may be accompanied by visual impairment, focal neurological deficits, seizures, or signs of raised intracranial pressure. Neuroimaging (MRI or CT venography) of the cerebral veins and dural sinus is used to establish the diagnosis. The mainstay of management is anticoagulation alongside the treatment of any potential underlying cause (e.g., antibiotics for septic CVT). Surgical intervention (e.g., endovascular thrombolysis or decompressive craniectomy) may be necessary in patients with significant symptoms who do not respond to anticoagulation.
- Cerebral venous thrombosis (CVT) or cerebral venous sinus thrombosis (CVST): a thrombotic obstruction of the cerebral veins and/or related anatomical structures (dural sinuses) which drain blood from the brain. Common subtypes include transverse sinus thrombosis and superior sagittal sinus thrombosis. 
- Septic cerebral venous thrombosis: a subtype of CVT of infectious origin (see “Etiology”).
- Cavernous sinus thrombosis: a rare subtype of CVT, typically septic in origin, that is associated with cavernous sinus syndrome.
- Hypercoagulable states
- Head trauma
- Neurosurgical procedures (e.g., )
- Additional associated systemic conditions
- Inflammatory bowel disease (e.g., Crohn's disease)
- Collagen vascular diseases and blood vessel disorders (e.g., lupus erythematosus, granulomatosis with polyangiitis, temporal arteritis)
- Hematologic conditions (e.g., paroxysmal nocturnal hemoglobinuria, thrombotic thrombocytopenic purpura, sickle cell disease)
- Nephrotic syndrome
- Rhinogenic (e.g., after sinusitis - paranasal, sphenoid, maxillary, and ethmoid)
- Mid-facial infections (cellulitis or abscess)
- Dental infections
- Otogenic (e.g., after acute otitis media) → generally infection of the lateral sinuses (transverse/sigmoid sinuses) or mastoiditis
- Orbital and periorbital cellulitis
- Thrombogenesis occurs in the cerebral venous system, including the dural sinuses → ↓ cerebral drainage → ↑ intracranial pressure → clinical features; ; (see below) 
- Additionally, thrombus formation → congestion within the venous system of the brain → blood stasis → ↓ oxygenated blood in brain tissue → cerebral edema and/or infarcts/stroke 
Symptoms vary depending on the size and location of the thrombosis. They are often nonspecific and may be masked by the underlying disorder(s), necessitating a high degree of clinical suspicion. Patients may have any symptoms of increased ICP or cerebral ischemia. 
- Most common symptom (∼ 90% of patients)
- Acute, subacute, or chronic
- May progress in severity over days or weeks
- Signs associated with intracranial hypertension
- Seizures (focal or generalized) 
- Signs of cranial nerve dysfunction, including: 
- Other focal neurological symptoms
- Behavioral changes (e.g., delirium, amnesia)
Since the thrombus develops gradually, clinical symptoms usually appear progressively and vary in magnitude.
- MRI head with MR venography (MRV): modality of choice (highest sensitivity) 
- CT head with CT venography (CTV): if MRI is unavailable or is contraindicated
- Findings: Typically similar in CTV and MRV
- Absence of flow in venography (Evidenced by filling defect in a vein or sinus)
- Intraluminal venous thrombus
- Focal edema secondary to ischemia
- Intraparenchymal hemorrhage
- Empty delta sign
- Direct cerebral venography: if MRV/CTV are inconclusive or for procedural planning. Findings include filling defects and venous congestion
- Noncontrast head CT
Additional evaluation 
- Routine laboratory studies
Additional studies to consider: to evaluate underlying etiology or complications
- CRP and blood cultures 
- Lumbar puncture 
- ESR and antibody studies
- Liver function tests 
- Thrombophilia screening: see “Diagnostics” in hypercoagulable states 
- EEG: if seizures are present
Posterior reversible encephalopathy syndrome (PRES) 
- Definition: a neurologic condition characterized by vasogenic edema in the subcortical white matter, especially in the posterior cerebral hemispheres
- Pathophysiology: The exact pathophysiology of PRES is not fully understood, but the following theories have been proposed.
- Clinical features: severity of symptoms may vary
- Complete recovery over days to weeks occurs in approx. 80% of cases
Other differential diagnoses
The differential diagnoses listed here are not exhaustive.
Initial management consists of general stabilization procedures (control of seizures, administration of fluids, treatment of intracranial hypertension) and treatment of the underlying cause. All patients require anticoagulation, and those with underlying infection require antimicrobial therapy. Surgical intervention should be considered if there is no improvement with medical therapy.
Medical management 
- Anticoagulation: indicated for all patients with CVT (intracerebral hemorrhage and underlying infection are not absolute contraindications) 
- Empiric antibiotic therapy: only indicated for suspected septic CVT (see also ).
- Fluid resuscitation
- Consider anticonvulsants: Indicated in patients with a seizure and supratentorial lesions on imaging, otherwise not routinely recommended. 
- Consider corticosteroids in the following:
Invasive procedures 
- Endovascular interventions
- Identify and treat any life-threatening complications.
- Obtain MRI/MRV to confirm the diagnosis (CT venography if MRV unavailable)
- Emergency neurology consult
- Start anticoagulation (e.g., heparin).
- Identify and treat underlying etiology, e.g., empiric IV antibiotics for septic CVT
- Begin neuroprotective measures and ICP management as needed.
- Monitor with serial neurological examination (e.g., GCS, visual field examination).
- If neurological deterioration despite therapeutic anticoagulation , urgent interventional radiology and/or neurosurgery consult for invasive treatment
- Consider ICU/stroke unit admission