Venous Infarct of the Brain (Cerebral Venous Thrombosis / CVT)

1. Overview & Epidemiology

• Most common in adult women, especially in association with pregnancy, the puerperium, and oral contraceptive use
• Also occurs in neonates and young infants (about half of paediatric cases)
• Rare but recognized complication of SARS-CoV-2 infection
• Incidence ~0.08% among hospitalized patients

Bradley and Daroff's Neurology in Clinical Practice — CVT constitutes 0.5–1% of all strokes; most modern cases involve adult women with puerperium or pregnancy-related risk factors.

2. Anatomy of Cerebral Venous Drainage

3. Pathophysiology

Why venous infarct differs from arterial infarct

1. Sinus/vein thrombosis → outflow obstruction
2. → Venous hypertension upstream in draining veins
3. → Impaired perfusion pressure (arteries still deliver blood but it cannot drain)
4. → Vasogenic oedema (interstitial fluid leaks from congested capillaries)
5. → Blood-brain barrier breakdown → haemorrhagic transformation (very common — much more so than arterial infarct)
6. → Eventually cytotoxic oedema and infarction if untreated

• Venous infarcts are frequently haemorrhagic (fragmented, petechial haemorrhage into congested tissue)
• They do not respect arterial territory boundaries
• They are often multifocal and bilateral
• Both grey matter and subcortical white matter are affected (cortex + immediate subcortex)
• Cerebral oedema is paradoxically less prominent than in large arterial infarcts

Grainger & Allison's Diagnostic Radiology — "Reduction in parenchymal venous drainage leads to venous hypertension and subsequent infarction, which is frequently haemorrhagic."

4. Causes & Risk Factors

• Cavernous sinus thrombosis: complication of facial/orbital infection → proptosis, chemosis, painful ophthalmoplegia
• Lateral sinus thrombosis: complication of otitis media/mastoiditis → headache, fever, otalgia, vertigo, papilledema, abducens palsy

Patients should be screened for thrombophilia after CVT.

5. Clinical Presentation

Symptoms by mechanism:

• Headache (most common symptom — present in >90%) — typically diffuse, progressive, worsening over days
• Vomiting
• Papilledema
• Transient visual obscurations
• Sixth nerve palsy (false localising)

• Hemiparesis or paraparesis (bilateral leg weakness in SSS thrombosis — affects parasagittal motor cortex)
• Hemisensory loss
• Aphasia
• Hemianopia
• Alternating focal deficits (unusual for arterial stroke)

• Focal or generalised seizures — very common, more so than arterial stroke

• Lethargy, stupor, coma
• Bilateral thalamic infarction (straight sinus/internal cerebral vein thrombosis) → coma, memory loss

Adams and Victor's Principles of Neurology — "A slower evolution of the stroke syndrome than with arterial occlusion strokes, multiple cerebral lesions not in arterial territories, and a convulsive and hemorrhagic character favor venous over arterial thrombosis."

6. Syndromes by Location

7. Imaging

CT (Non-contrast)

• Dense/hyperdense sinus or vein = acute clot (the "dense triangle sign" in SSS)
• "Cord sign" = hyperdense thrombosed cortical vein on plain CT
• Haemorrhagic infarction in a non-arterial distribution
• Small ventricles (cerebral swelling)

CT with contrast (CT Venography)

• Empty delta sign (empty triangle sign): triangular filling defect (hypodense clot centre) surrounded by enhancing dural walls in the posterior SSS — the most classic CT sign
• Filling defect within sinus on CTV
• Absent opacification of sinus confirms thrombosis

MRI

• Loss of normal flow void in the sinus (normally seen as black stripe)
• Thrombosed sinus can be hyperintense on T1 and T2 (subacute thrombus — methhaemoglobin)
• Very acute thrombus can be hypointense on T2 (deoxy-Hb) — can mimic normal flow void (pitfall!)
• FLAIR/T2: high signal (oedema) in venous territory ± haemorrhage

SWI (Susceptibility-Weighted Imaging) — most sensitive

• "Blooming" = exaggerated hypointensity of thrombosed vein/sinus (beyond expected size)
• Multiple prominent serpiginous veins in the congested territory = venous hypertension
• Identifies acute haemorrhage
• Phase images can identify occluded cortical veins

MR Venography (MRV) — the gold standard

• Loss of flow signal in affected sinus
• Absence or irregularity of venous flow confirms thrombosis
• Has replaced conventional angiography for diagnosis
• Useful also for follow-up and recanalisation assessment

• SSS → bilateral (often asymmetric) cortical/subcortical lesions, parasagittal, parietal/frontal
• Lateral sinus → posterolateral temporal lobe, inferior parietal lobule
• Straight sinus/internal cerebral vein → bilateral thalami ± basal ganglia
• Vein of Labbé → anterolateral right temporal lobe

8. Imaging Examples

Cord Sign (MRI) + Empty Delta Sign (CTV)

CVT with Haemorrhagic Infarction (Multi-modality from Grainger & Allison)

9. Diagnosis

1. Clinical suspicion — headache + seizures + encephalopathy or stroke in young woman, peripartum, or OCP user
2. CT/NECT — quick screening; look for dense sinus, dense cortical vein, non-arterial haemorrhage
3. CT venography — excellent for major dural sinuses; shows empty delta, filling defects
4. MRI + MRV — preferred combination; better for parenchymal lesions and small cortical veins
5. SWI — most sensitive for cortical vein thrombosis
6. DSA (conventional angiography) — now rarely needed; reserved for endovascular therapy planning
7. CSF — raised opening pressure; may be xanthochromic; not required for diagnosis
8. Thrombophilia screen — essential after diagnosis

MRV alone can be misleading (hypoplastic sinus vs thrombosis vs slow flow). Correlation with T1/T2/SWI is essential.

10. Treatment

Anticoagulation — cornerstone (even with haemorrhagic infarction)

ICP Management

• Acetazolamide, repeated LP for raised ICP
• Head elevation, hyperventilation (short-term)
• Avoid hyperosmolar therapy if significant oedema

Anticonvulsants

• Prophylactic or therapeutic seizure medications (especially if cortical involvement/seizures present)

Antibiotics

• For septic CVT only

Escalation if deteriorating:

• Local sinus thrombolysis (urokinase/tPA via catheter) — if failing anticoagulation
• Mechanical thrombectomy of occluded sinus — endovascular option
• Decompressive craniectomy — for malignant oedema/herniation (life-saving in selective cases)

Bradley and Daroff's — "The efficacy of heparin has been shown even in patients who have evidence of intracranial hemorrhage by neuroimaging studies."

11. CVT vs Arterial Infarct — Key Differences

12. Prognosis

• Most patients with prompt anticoagulation have good outcomes
• Mortality ~5–10% in modern series
• Recanalisation occurs in a majority
• Risk of recurrent thromboembolism — screen for underlying hypercoagulability
• Long-term anticoagulation depends on underlying cause (provoked vs unprovoked, persistent risk factors)

• Bradley and Daroff's Neurology in Clinical Practice (Chapter 65)
• Adams and Victor's Principles of Neurology, 12th Edition (Chapter 33)
• Grainger & Allison's Diagnostic Radiology (Chapter 56)
• Goldman-Cecil Medicine, 26th Edition (Chapter 376)
• Neuroanatomy through Clinical Cases, 3rd Edition (Case 10.13)