Normal Anatomy, physiology, and anatomical variants

The cerebral venous system plays a crucial role in draining deoxygenated blood from the brain parenchyma, maintaining intracranial pressure balance, and facilitating the clearance of metabolic waste. Unlike the arterial system, cerebral veins lack valves, allowing bidirectional flow and making them susceptible to thrombosis in states of altered haemodynamics.

The cerebral venous system consists of:

• Dural venous sinuses: Superior sagittal sinus, transverse sinus, straight sinus. These large endothelial lined channels collect blood from the superficial and deep venous systems and drain into the internal jugular veins.The superior sagittal sinus primarily drains the superficial cortical veins. The straight sinus collects blood from the deep venous system via the vein of Galen. The transverse and sigmoid sinuses facilitate venous drainage into the internal jugular vein.
• Deep venous system: Comprising the internal cerebral veins, vein of Galen, and basal veins of Rosenthal, this system is responsible for draining the deep structures of the brain, including the thalamus, basal ganglia and deep white matter structures.
• Superficial veins: Vein of Trolard, vein of Labbé, superficial middle cerebral vein. Ensure drainage of cortical regions into the dural sinuses. The vein of Trolard primarily drains the superior parts of the cerebral hemispheres, connecting the superficial veins with the superior sagittal sinus. The vein of Labbé facilitates drainage of the temporal lobe, directing blood towards the transverse sinus. The superficial middle cerebral vein follows the lateral sulcus (Sylvian fissure), draining blood from the lateral aspects of the frontal, temporal, and parietal lobes, eventually emptying into the cavernous sinus.

Fig 4: Illustrations of the dural sinuses and superficial and deep veins (star) in sagittal (A), coronal (B), and axial (C) planes, with their corresponding drainage territories. 1.Superior sagittal sinus 2.Transverse sinuses 3.Sigmoid sinuses 4. Inferior sagittal sinus 5. Confluence of sinuses (torcular Herophili) 6.Veins of Trolard 7.Veins of Labbé 8.Frontal cortical veins 9.Straight sinus 10.Vein of Galen 11. Internal cerebral veins 12.Basal veins of Rosenthal 13. Jugular veins.

Common anatomical variants (Figure 5):

• Hypoplasia of the transverse sinus (Figure 6).
• Arachnoid granulations within the venous sinuses, mimicking filling defects .
• Asymmetry of the sigmoid and transverse sinuses.
• Fenestration of the superior sagittal sinus, which may alter normal flow dynamics.
• Duplication of the internal cerebral veins, which can be mistaken for pathological findings.
• Persistent embryological venous structures, such as a persistent falcine sinus or an unpaired para midline vein.

Fig 5: Illustration: Coronal view of anatomical variants of the superior sagittal sinus and transverse sinuses. Normal confluence Bifurcation Hypoplasia of the right transverse sinus Hypoplasia of the left transverse sinus

Fig 6: Examples of anatomical variants of the venous sinuses that may lead to a false-positive diagnosis (A) Illustration of transverse sinus bifurcation. (B) Contrast-enhanced CT scan of a patient with transverse venous sinus bifurcation, which could be misinterpreted as a delta sign (arrow). (C) Illustration of a hypoplastic left transverse sinus, the most common anatomical variant. (D) Coronal contrast-enhanced CT scan, demonstrating the left transverse sinus (arrow). (E) Coronal T1-weighted sequence with gadolinium from the same patient as in (D), showing the anatomical variant.

Key Imaging Findings of CVT

Magnetic resonance imaging (MRI) in combination with MR venography is considered the gold standard technique for diagnosing CVT, as it allows direct identification of the venous thrombus and secondary parenchymal changes. However, CT is the most widely used imaging modality in the emergency setting and can detect both direct and indirect signs of CVT. Time of flight (TOF) MR venography is particularly useful for non contrast assessment of venous flow dynamics, as it enables detection of flow void absence in thrombosed venous structures. 

Recommended MRI protocol:

• T1 and T2 weighted sequences: Assess thrombus signal changes.
• FLAIR and DWI/ADC: Detect venous oedema and infarctions.
• T2-GRE or SWI: Evaluate venous haemorrhage.
• Contrast-enhanced MRV: Gold standard for thrombosis evaluation.

CVT leads to a progressive obstruction of venous outflow, resulting in increased venous pressure, congestion, and potential venous infarction. The imaging findings can be categorised into direct and indirect signs, reflecting the underlying pathophysiology of the disease. 

Direct signs on CT and MRI: Direct signs of CVT reflect the presence of an intravascular thrombus (Figure 7 , 8 and 9):

• Dense cord/clot sign (CT): Hyperattenuated appearance of the thrombosed venous sinus or cortical veins due to acute clot formation, best observed in non contrast CT.

• Filling defect on contrast enhanced in venous sinuses or cortical veins (CT / MRI) (Figure 9).
  

  Fig 9: Direct Signs of Cerebral Venous Thrombosis A 60-year-old female patient with a history of hypertension presented to the emergency department with headache unresponsive to analgesia and lower limb weakness. A non-contrast CT scan was performed, showing no abnormalities. However, due to persistent symptoms, the patient was admitted for observation, and a brain MRI was requested, revealing extensive thrombosis of the right dural sinuses, involving the torcular Herophili, transverse sinus, sigmoid sinus, and extending to the ipsilateral internal jugular vein. (A) Axial T1 weighted sequence with gadolinium: Demonstrates a filling defect in the right sigmoid sinus (arrow). (B) Shows a filling defect in the ipsilateral transverse sinus (arrow). (C) Sagittal view. Empty delta sign: Suggestive of thrombosis in the torcular Herophili and superior sagittal sinus (arrow). Antithrombotic treatment was initiated, and a follow up MRI performed six months later showed recanalisation of the previously affected dural sinuses. (D) Axial T1 weighted sequence with gadolinium: Evidence of recanalisation of the right sigmoid sinus (arrow). (E) Shows recanalisation of the right transverse sinus (arrow). (F) Sagittal view: Demonstrates recanalisation of the torcular Herophili and superior sagittal sinus (arrow). The patient showed good clinical recovery with no residual neurological deficits.

• Empty delta sign (CT / MRI): A contrast enhanced periphery surrounding a filling defect within the superior sagittal sinus, representing collateral circulation and central non opacification due to thrombus. On MRI, it appears as a signal void on post contrast T1 weighted imaging due to the lack of contrast opacification, with surrounding dural enhancement.
  

  Fig 10: Empty delta sign
• Absence of signal void (MRI T2): Normally, venous sinuses appear as flow voids on T2 weighted sequences. A thrombosed sinus lacks this flow void due to stagnant blood, indicating obstruction.
• Hypointense thrombus on T2 GRE/SWI (MRI): Subacute or chronic thrombus contains deoxygenated haemoglobin or haemosiderin, leading to blooming artefact due to paramagnetic effects.
• Hyperintense thrombus on T1/T2 (MRI): In the subacute phase, methaemoglobin accumulation results in a hyperintense signal within the thrombosed sinus.

Fig 7: Non contrast CT findings of cortical venous thrombosis. (A) Hyperdense clot sign: Axial CT scan showing a hyperdensity in the superior left cortical vein (arrow). (B) Coronal view: The hyperdense clot sign is associated with vasogenic oedema (arrow). (C) Sagittal view: Confirms the presence of the hyperdense clot sign, further supporting the diagnosis (arrow).

Fig 8: Contrast-enhanced CT and progression of complications in the same patient as the figure 7. (D) Vasogenic oedema. Axial CT scan demonstrating gyral swelling in the superior left frontal sulci (arrow), leading to the decision to perform contrast-enhanced CT. (E) Segmental lack of contrast enhancement: Involvement of the superior left frontal cortical veins, consistent with cortical venous thrombosis (arrow). (F) Complication – Intraparenchymal haemorrhage: The patient developed a haemorrhagic transformation, requiring urgent decompressive craniectomy.

Indirect signs on CT and MRI: Indirect signs of CVT arise from impaired venous drainage, leading to venous congestion, ischaemia, and haemorrhagic transformation. These secondary changes can significantly affect brain parenchyma:

• Venous infarction (CT/ MRI): Venous infarctions occur due to impaired venous drainage, leading to increased capillary pressure, blood brain barrier disruption, and subsequent oedema or haemorrhage. Unlike arterial infarcts, which follow specific vascular territories, venous infarctions are often non territorial and may cross arterial boundaries.The typical distribution of venous infarctions varies depending on the affected venous structure:

- Superior sagittal sinus thrombosis: Parasagittal infarcts in the frontal and parietal lobes.

- Transverse and sigmoid sinus thrombosis: Infarcts in the temporal and occipital lobes.

- Deep venous system thrombosis (vein of Galen, internal cerebral veins, straight sinus): Bilateral thalamic and basal ganglia infarcts.

- Cortical vein thrombosis: Isolated cortical or subcortical infarcts that do not conform to arterial territories.

Fig 11: The typical distribution of venous infarctions varies depending on the affected venous structure.

On CT, venous infarctions appear as hypodense regions with possible haemorrhagic transformation, seen as hyperdense foci. Unlike arterial infarcts, which primarily exhibit cytotoxic oedema, venous infarctions frequently show mixed vasogenic and cytotoxic oedema, leading to a more diffuse involvement.

On MRI, venous infarctions appear hyperintense on T2/FLAIR, reflecting oedema, and may show restricted diffusion on DWI/ADC, though this pattern is often less pronounced than in arterial infarcts. Haemorrhagic components are best visualised on T2 GRE/SWI, where blooming artefacts indicate blood products. Contrast enhancement in the subacute phase may occur due to blood-brain barrier breakdown. 

• Vasogenic oedema (MRI): Due to venous congestion, affected areas develop interstitial fluid accumulation, appearing as hyperintense regions on T2 weighted and FLAIR sequences.
• Tentorial and cortical venous enhancement (CT/MRI): Collateral circulation develops around thrombosed venous structures, leading to abnormal contrast enhancement of the cortical and tentorial veins.
• Subarachnoid haemorrhage and subdural haematomas (CT/MRI): Venous congestion weakens vessel walls, predisposing them to rupture. Haemorrhagic complications can appear as subarachnoid or subdural collections.

Common Diagnostic PitfallsFalse Positives

• Arachnoid granulations: Normal structures within the venous sinuses that can appear as small filling defects (Figure 12).
• Flow artifacts in MR venography: Slow or turbulent flow can create pseudo-defects, mimicking thrombosis (Figure 13).
• Incorrect contrast bolus timing: Incomplete opacification of venous sinuses may lead to misinterpretation as thrombosis.
• Asymmetric venous sinuses: Common anatomical variants, such as unilateral hypoplasia of the transverse sinus, which can be mistaken for pathology.

Fig 12: Arachnoid Granulations. It is essential to consider the absence of both direct and indirect signs of cerebral venous thrombosis, as well as the patient's clinical presentation, to avoid false-positive diagnoses. (A) Coronal and (B) Sagittal contrast-enhanced CT scans: A small filling defect is observed in the superior sagittal sinus, which could be mistaken for dural sinus thrombosis. However, MRI confirmed the finding as an arachnoid granulation. (C) Coronal and (D) Sagittal T1-weighted MRI sequences with contrast: Confirmation of an arachnoid granulation.

Fig 13: Flow Artifact. Flow-related artifacts may mimic cerebral venous thrombosis, leading to false-positive diagnoses. To minimise this, it is recommended to perform contrast-enhanced MR venography, avoid TOF sequences in planes parallel to venous flow, and use SWI/T2-GRE sequences to detect acute thrombosis. (A) T2-weighted sequence: Hypointense signal alteration in the right sigmoid sinus (arrow). (B) T1-weighted sequence: Hyperintense right sigmoid sinus (arrow). (C) Despite these findings, there is no corresponding hypointensity on gradient-echo imaging nor any parenchymal signal alteration, suggesting turbulent/slow flow rather than intracranial venous thrombosis (arrow).

False Negatives

• Subacute or chronic thrombus with altered signal intensity: In later stages, thrombi may become isointense to surrounding structures, making them difficult to detect on standard imaging sequences.
• Use of inappropriate imaging sequences: Lack of GRE/SWI sequences may miss paramagnetic effects of blood products, reducing sensitivity for chronic thrombi.
• Non contrast CT in early thrombosis: In the acute phase, thrombi may not be sufficiently hyperattenuated, leading to underdiagnosis if contrast-enhanced imaging is not performed.
• Small cortical vein thrombosis: These may be overlooked due to their subtle imaging findings and the absence of associated venous infarcts.

Complications

CVT can lead to severe complications if not promptly diagnosed and treated:

• Venous infarction: Resulting in haemorrhagic stroke due to increased venous pressure.
• Intracranial haemorrhage: Including subarachnoid, subdural, and intraparenchymal bleeding.
• Intracranial hypertension: Due to impaired venous drainage, leading to papilloedema and vision loss.
• Cerebral herniation: In severe cases with extensive oedema and mass effect.

Fig 14: 71-year-old patient with a history of ovarian cancer presents to the emergency department with seizures. A non-contrast CT scan is performed, revealing: (A) Sagittal CT scan: Dense cord sign in the left superior cortical veins (arrow), with mild associated oedema, suggesting cortical venous thrombosis. (B) Axial CT scan: Dense cord sign is also observed. The following day, a follow-up CT scan is performed, showing: (C) Axial CT scan: Persistence of the hyperattenuating cord sign (arrow), now associated with increased vasogenic oedema (*). (D) Haemorrhagic transformation as a complication. Axial CT scan: Established left frontoparietal infarction with haemorrhagic transformation, which was not evident on the previous day’s CT scan (E).