A. Key Radiological Signs IA must detect

1. Dural Sinus Thrombosis

Dural sinus thrombosis is the most common form of CVT, involving the dural venous sinuses that drain blood from the brain to the internal jugular veins.

• Direct Signs:

  • Cord Sign: Hyperattenuating thrombosed vein or sinus on non-contrast CT, representing acute thrombus.
  • Empty Delta Sign: Hypoattenuating thrombus surrounded by enhancing dural sinuses on contrast-enhanced CT.

• Parenchymal Findings:

  • Vasogenic edema or venous infarcts in the regions drained by the affected sinuses, such as the frontal or parietal lobes (non arterial distribution).
  • Hemorrhagic transformation, often irregular and in a venous distribution.
    
    

• Pitfalls:

  • Arachnoid Granulations: Can mimic filling defects on contrast-enhanced studies.
  • Hypoplastic or Asymmetric Sinuses: Variants that may be misinterpreted as thrombotic changes.
  • High location of Torcula.
    

2. Deep Cerebral Vein Thrombosis (DCVT)

DCVT involves the occlusion of deep venous structures, such as the internal cerebral veins or basal veins of Rosenthal.

• Key Signs:

  • Bilateral Thalamic Edema: A hallmark finding caused by venous congestion, which may extend to the basal ganglia.
  • Hemorrhagic Infarctions: Often in deep venous territories, accompanied by cytotoxic and vasogenic edema.
  • Hiperdensity of deep veins.
  • Hydrocephalus due to compression of the foramen of Monro.
    

• Pitfalls:
  • Thrombosis Mimicking Other Pathologies: Bilateral thalamic edema can also be seen in pathologies such as hypoxic-ischemic injury, artery of Percheron infarction, or metabolic disorders, which may lead to diagnostic confusion.
  • Hemorrhagic Transformations: Can resemble other causes of intracerebral hemorrhage, such as hypertension or coagulopathy, especially in atypical locations.
    

3. Isolated Cortical Vein Thrombosis

This rare type of CVT affects the cortical veins without involving major dural sinuses.

• Key Signs:

  • Hyperattenuating Cortical Veins on CT ("Cord Sign"): Reflects acute thrombosis within superficial cortical veins.
  • Subcortical Edema or Hemorrhage: Found adjacent to the affected veins, often in atypical distributions.

• Pitfalls:

  • Adjacent edema can resemble tumors or other inflammatory proccess
  • Confusion with Subarachnoid Hemorrhage (SAH): Cortical vein thrombosis may cause small sulcal hemorrhages.
  • Hemorrhagic Contusions: Focal hemorrhages resembling traumatic contusions.
    
    
    

4. Cavernous Sinus Thrombosis (CST)

CST involves the cavernous sinus and is often associated with infections, such as sinusitis or facial cellulitis.

• Key Signs:

  • Enlargement and hypoattenuation of the cavernous sinus with filling defects.
  • Associated findings, including proptosis, ophthalmoplegia, and superior ophthalmic vein thrombosis.

• Imaging Techniques:

  • Contrast-enhanced CT or MRI are essential for evaluation, particularly to assess venous involvement and potential infectious sources.
    
    

B. Critical Scenarios Requiring AI Alertness

AI systems must prioritise the following clinical situations:

1. Local Factors

These factors directly compromise the cerebral venous system, often leading to thrombosis through mechanical injury or local inflammation:

• Cranioencephalic Trauma (CET): Fractures involving the skull base or dural venous sinuses can lead to venous injury and subsequent thrombosis.
  
• Local Infections:
  • Otitis and Mastoiditis: Infection spreading from the middle ear or mastoid air cells to adjacent venous sinuses can trigger thrombosis.
    
  • Sinusitis and Meningitis: These infections can lead to direct involvement of venous sinuses or veins via inflammatory mediators and septic emboli.
• Brain Tumors:
  • Mass effect or direct invasion of venous structures by tumors can cause venous obstruction.
  • Peritumoral edema and radiotherapy further increase the risk of venous thrombosis.
• Recent Neurosurgery/Endovascular intervention
  
  
• Anatomical alterations that impair venous flow
  

2. Systemic Factors

Systemic conditions predispose patients to a hypercoagulable state, increasing the likelihood of thrombus formation:

• Hypercoagulable States:
  • Pregnancy and Postpartum: Hormonal and hemodynamic changes significantly elevate the risk of CVT, especially during the postpartum period.
  • Oral Contraceptives: Estrogen-containing contraceptives are a known risk factor, particularly in women with other prothrombotic conditions.
    
    
• Recent Surgery: Postoperative states, especially after neurosurgery or prolonged immobilization, increase thrombotic risk due to venous stasis and endothelial injury.
• Hematologic Disorders:
  • Hereditary Thrombophilia: Conditions such as Factor V Leiden mutation or prothrombin gene mutations predispose to venous thrombosis.
  • Acquired Thrombophilia: Examples include antiphospholipid syndrome or malignancy-associated coagulopathy.
    
    
• Severe Dehydration: Particularly common in children or elderly patients, dehydration can cause hemoconcentration and venous stasis, promoting thrombosis.
• Malignancies: Advanced-stage cancers, especially those with high prothrombotic potential (e.g., pancreatic or gastric cancer), are a significant systemic risk factor.

3. Idiopathic Cases: In up to 20% of CVT cases, no clear risk factor can be identified. These patients present a diagnostic challenge and highlight the need for vigilance in atypical presentations.