Cerebral Venous Sinus Thrombosis (CVST - Empty Delta Sign & Venous Infarction)

• Seen in young to middle-aged adults (peak age 20–45 years; female:male 3:1, strong association with oral contraceptive use, pregnancy / puerperium, dehydration, systemic prothrombotic conditions [Factor V Leiden, antiphospholipid syndrome], COVID-19, and adjacent skull base / mastoid infections) presenting with severe, progressive 'thunderclap' or subacute persistent headache, papilledema, seizures, focal neurological deficits, and altered consciousness.
• Caused by thrombotic occlusion of the dural venous sinuses and/or cerebral cortical veins:
• (1)
  Anatomical Distribution: Superior Sagittal Sinus (SSS, 60%), Transverse Sinus (45%), Sigmoid Sinus (40%), Straight Sinus (15%), and Deep Cerebral Internal Veins (10%).
• (2)
  Pathophysiological Cascade:
• 1.
  Venous Congestion: Occlusion increases venous and capillary hydrostatic pressure, disrupting the blood-brain barrier and causing profound vasogenic edema.
• 2.
  Venous Infarction & Hemorrhage: Elevated capillary pressure leads to capillary rupture, causing petechial microhemorrhages that coalesce into typical non-arterial, hemorrhagic venous infarctions.
• 3.
  Impaired CSF Resorption: Occlusion of arachnoid granulations in the SSS impairs CSF resorption, triggering severe intracranial hypertension.

Imaging Findings

• Computed Tomography (Non-Contrast Head CT & CTV Protocol):
• –
  Non-Contrast CT Signs:
• 1.
  The 'Dense Triangle' or 'Cord' Sign: Hyperdense, freshly clotted acute thrombus within the lumen of the superior sagittal sinus or cortical vein (typically 60–80 HU) on unenhanced scans.
• 2.
  Atypical Non-Arterial Infarction: Segmental, bilateral, or parasagittal edema with flame-shaped cortical/subcortical hemorrhage that DOES NOT respect any arterial vascular territory.
• –
  Contrast-Enhanced CT / CT Venography (CTV - Diagnostic Gold Standard):
• 1.
  The 'Empty Delta' Sign: Pathognomonic triangular intraluminal filling defect within the posterior superior sagittal sinus, created by non-enhancing central thrombus surrounded by brightly enhancing collateral dural channels and cavernous spaces in the sinus wall.
• 2.
  Abrupt Venous Cutoff: Complete non-opacification of a major dural venous sinus on 3D CTV.
• Magnetic Resonance Imaging & MR Venography (MRI / MRV - High-Sensitivity Protocol):
• –
  Evolution of Thrombus Signal:
• 1.
  Acute (0–5 days): Iso-intense on T1, dark/hypointense on T2 (mimicking normal flow void, verified on MRV).
• 2.
  Subacute (6–15 days): Pathognomonically bright / hyperintense on BOTH T1WI and T2WI due to intracellular and extracellular methemoglobin.
• 3.
  Susceptibility-Weighted Imaging (SWI): Dramatic, blooming signal void outlining the thrombosed cortical veins ('tram-track' or 'brush' sign).
• –
  Time-of-Flight MR Venography (2D TOF MRV): Absence of normal hyperintense flow signal in the occluded sinus.
• –
  DWI / ADC: Venous congestion produces mixed vasogenic edema (elevated ADC, potentially reversible) and cytotoxic edema (true diffusion restriction with low ADC) in a non-arterial distribution; the intraluminal thrombus itself can also show high DWI signal.
• –
  **SWI / T2* GRE: Essential sequence—demonstrates marked intraluminal blooming artifact within the thrombosed dural sinus or cortical vein (especially critical for isolated cortical vein thrombosis) and flame-shaped hemorrhagic venous infarction** in the parasagittal or temporal parenchyma.

Differential Diagnosis

Important Points to Remember

• Diagnostic Pitfall: Withholding therapeutic anticoagulation because the patient has an intracranial hemorrhage! In arterial stroke, intracranial hemorrhage is an absolute contraindication to therapeutic anticoagulation. In cerebral venous sinus thrombosis, the hemorrhage is a secondary VENOUS hemorrhagic infarction caused by downstream outflow obstruction. Full-dose therapeutic anticoagulation (unfractionated or low-molecular-weight heparin) is MANDATORY and life-saving even in the presence of extensive intracranial venous hemorrhage, as halting thrombus propagation restores outflow and reduces venous hypertension.
• Crucial Review Areas:
• 1.
  Posterior aspect of the Superior Sagittal Sinus on axial CTV for the pathognomonic 'Empty Delta Sign'.
• 2.
  Cortical veins on SWI / GRE for blooming susceptibility signal confirming cortical venous thrombosis.
• 3.
  Mastoid air cells and middle ear cavities on bone windows to exclude coalescent mastoiditis triggering secondary sigmoid sinus septic thrombophlebitis.
• 4.
  Deep cerebral internal veins (Vein of Galen, straight sinus) in patients presenting with coma or bilateral thalamic edema.
• Radiologist Safe Practice & Management:
• 1.
  Immediate Critical Verbal Alert: Instant telephone notification to the Acute Stroke / Neurology Team and Neuro-Intensive Care Unit; CVST is a medical emergency requiring rapid intervention.
• 2.
  Immediate Therapeutic Anticoagulation: Full therapeutic anticoagulation with subcutaneous Low-Molecular-Weight Heparin (LMWH, e.g. Enoxaparin 1 mg/kg BD) or IV Unfractionated Heparin, REGARDLESS of the presence of intracranial hemorrhagic infarction.
• 3.
  Intracranial Pressure (ICP) Management: Elevation of head of bed, Osmotherapy (Mannitol or hypertonic saline), and seizure prophylaxis with Levetiracetam if seizures occur.
• 4.
  Endovascular Thrombectomy / Thrombolysis: Catheter-directed mechanical thrombectomy or intrasinus thrombolysis reserved for patients exhibiting neurological deterioration despite therapeutic heparin.
• 5.
  Long-Term Anticoagulation & Thrombophilia Screening: Transition to oral anticoagulation (Warfarin [INR 2.0–3.0] or DOACs) for 3–12 months, combined with formal outpatient thrombophilia workup.