Cerebral venous infarction is an uncommon form of stroke, and is most commonly secondary to cerebral venous thrombosis and frequently manifests with haemorrhage. It should be considered in infarcts (with or without haemorrhage) which do not correspond to a typical arterial territory 1.
No particular factors have been identified in patients predisposed to venous infarct / haemorrhage following venous sinus thrombosis. Please refer to the article on cerebral sinus thrombosis for a general discussion on epidemiology and risk factors.
Other causes of venous occlusion should also be considered (dural AVF, trauma, ligation).
Presentation may result in focal neurological deficits, or symptoms from mass effect/hydrocephalus if extensive oedema is present. If rapid decline in level of consciousness or cranial nerve palsies, deep venous infarcts affecting the brainstem should be considered.
Up to 50% of venous sinus thromboses will develop infarction and/or haemorrhage 2. The underlying mechanisms are still not well understood, with multiple factors compounding the main driver of venous congestion 3:
- increased venous pressure
- occlusion following thrombosis will increase local venous pressure and can lead to rupture of venules / capillaries
- cerebral veins also lack valves so back pressure can be demonstrated 2
- flow dynamics
- the increased venous pressure reduces effective drainage of affected brain tissue, with increased cerebral blood volume and reduced perfusion pressures, with subsequent oxygen debt and eventual infarction
- increased intracranial pressure
- this is seen less frequently and in more severe cases due to the collaterals of the venous system
- capillary recruitment
- in the reperfusion phase of infarct, the recruitment of immature capillaries are themselves friable and prone to infarct/haemorrhage
CT / MRI
Venous thrombosis should be considered in the assessment of confluent infarct or haemorrhage in atypical areas, crossing arterial territories, or infarcts with cortical sparing 4.
These are typically seen in parasagittal structures (following sagittal sinus thrombosis), temporoparietal regions (transverse / sigmoid sinus thrombi), or deep structures 4.
Haemorrhages typically start centrally and spread to the periphery of the affected lesion in venous infarcts 3.
See main venous thrombosis article.
Treatment and prognosis
Treatment is usually the same as for venous sinus thrombosis, with early anticoagulation initiation. The presence of haemorrhage is not a contraindication to anticoagulation, but should be reviewed and decided on a case basis 5,6.
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- 8. Kurokawa Y, Sohma T, Tsuchita H et-al. Findings of magnetic resonance imaging in cerebral venous occlusion: difference from hemorrhagic infarction. Comput Med Imaging Graph. 14 (6): 425-9. Pubmed citation
- 9. Forbes KP, Pipe JG, Heiserman JE. Evidence for cytotoxic edema in the pathogenesis of cerebral venous infarction. AJNR Am J Neuroradiol. 2001;22 (3): 450-5. AJNR Am J Neuroradiol (full text) - Pubmed citation