Cerebral venous infarction

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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.

Epidemiology

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).

Clinical presentation

Presentation may result in focal neurological deficits, or symptoms from mass effect / hydrocephalus if extensive oedema, but largely will follow presentation of venous sinus thrombosis. If rapid decline in level of consciousness or cranial nerve palsies, deep venous infarcts affecting the brainstem should be conisdered.

Pathology

CerebralUp 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 sever cases due to the good collateralisation of the venous system; overall drainage can usually be achieved via other pathways
  • capillary recruitment: in the reperfusion phase of infarct, the recruitment of immature capillaries are themselves friable and prone to infarct / haemorrhage

Radiographic features

CT / MRI

Venous thrombosis should be considered in the assessment of confluent infarct or haemorrhage in atypical areas or 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.

Venogram

See main venous thrombosis article.

Treatment and prognosis

Treatment is usually the sequelae of cerebral venous thrombosis, complicating both duralsame as for venous sinus thrombosis, with early anticoagulation initiation. The presence of haemorrhage is not a contraindication to anticoagulation, but should be reviewed and deep cerebral venous thrombosis. Any other cause of venous occlusion can also lead to venous infarction, including trauma and surgical ligation.

Asdecided on a result of the arterial supply to the infarcted tissue not being compromised, a haemorrhagic transformation is common and is typically heterogenous and gyriformcase basis 5,6.

Differential diagnosis

  • infiltrating glioma but will have a different evolution
  • -<p><strong>Cerebral venous infarction </strong>is an uncommon form of stroke, and is most commonly secondary to cerebral venous thrombosis. </p><h4>Pathology</h4><p>Cerebral venous infarction is usually the sequelae of <a href="/articles/cerebral-venous-thrombosis">cerebral venous thrombosis</a>, complicating both <a href="/articles/dural-venous-sinus-thrombosis">dural venous sinus thrombosis</a> and <a href="/articles/deep-cerebral-vein-thrombosis">deep cerebral venous thrombosis</a>. Any other cause of venous occlusion can also lead to venous infarction, including trauma and surgical ligation.</p><p>As a result of the arterial supply to the infarcted tissue not being compromised, a <a href="/articles/haemorrhagic-transformation">haemorrhagic transformation</a> is common and is typically heterogenous and gyriform.</p><h4>Differential diagnosis</h4><ul><li>infiltrating <a href="/articles/glioma">glioma</a> but will have a different evolution</li></ul>
  • +<p><strong>Cerebral venous infarction </strong>is an uncommon form of stroke, and is most commonly secondary to <a title="Cerebral venous thrombosis" href="/articles/cerebral-venous-thrombosis">cerebral venous thrombosis</a> and frequently manifests with haemorrhage. It should be considered in infarcts (with or without haemorrhage) which do not correspond to a typical arterial territory <sup>1</sup>.</p><h4>Epidemiology</h4><p>No particular factors have been identified in patients predisposed to venous infarct / haemorrhage following venous sinus thrombosis. Please refer to the article on <a title="Cerebral venous thrombosis" href="/articles/cerebral-venous-thrombosis">cerebral sinus thrombosis</a> for a general discussion on epidemiology and risk factors.</p><p>Other causes of venous occlusion should also be considered (<a title="Dural AVF" href="/articles/dural-arteriovenous-fistula">dural AVF</a>, trauma, ligation).</p><h4>Clinical presentation</h4><p>Presentation may result in focal neurological deficits, or symptoms from mass effect / hydrocephalus if extensive oedema, but largely will follow presentation of venous sinus thrombosis. If rapid decline in level of consciousness or cranial nerve palsies, deep venous infarcts affecting the brainstem should be conisdered.</p><h4>Pathology</h4><p>Up to 50% of venous sinus thromboses will develop infarction and/or haemorrhage <sup>2</sup>. The underlying mechanisms are still not well understood, with multiple factors compounding the main driver of venous congestion <sup>3</sup>:</p><ul>
  • +<li>
  • +<strong>increased venous pressure</strong>: 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 <sup>2</sup>
  • +</li>
  • +<li>
  • +<strong>flow dynamics</strong>: 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</li>
  • +<li>
  • +<strong>increased intracranial pressure</strong>: this is seen less frequently and in more sever cases due to the good collateralisation of the venous system; overall drainage can usually be achieved via other pathways</li>
  • +<li>
  • +<strong>capillary recruitment</strong>: in the reperfusion phase of infarct, the recruitment of immature capillaries are themselves friable and prone to infarct / haemorrhage</li>
  • +</ul><h4>Radiographic features</h4><h5>CT / MRI</h5><p>Venous thrombosis should be considered in the assessment of confluent infarct or haemorrhage in atypical areas or crossing arterial territories, or infarcts with cortical sparing <sup>4</sup>.</p><p>These are typically seen in parasagittal structures (following sagittal sinus thrombosis), temporoparietal regions (transverse / sigmoid sinus thrombi), or deep structures <sup>4</sup>.</p><p>Haemorrhages typically start centrally and spread to the periphery of the affected lesion in venous infarcts <sup>3</sup>.</p><h5>Venogram</h5><p>See main <a title="Cerebral venous thrombosis" href="/articles/cerebral-venous-thrombosis">venous thrombosis</a> article.</p><h4>Treatment and prognosis</h4><p>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 <sup>5,6</sup>.</p>

References changed:

  • 1. Saposnik G, Barinagarrementeria F, Brown RD, Bushnell CD, Cucchiara B, Cushman M, deVeber G, Ferro JM, Tsai FY. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. (2011) Stroke. 42 (4): 1158-92. <a href="https://doi.org/10.1161/STR.0b013e31820a8364">doi:10.1161/STR.0b013e31820a8364</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/21293023">Pubmed</a> <span class="ref_v4"></span>
  • 2. B. Schaller, R. Graf. Cerebral Venous Infarction: The Pathophysiological Concept. (2004) Cerebrovascular Diseases. 18 (3): 179. <a href="https://doi.org/10.1159/000079939">doi:10.1159/000079939</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/15273432">Pubmed</a> <span class="ref_v4"></span>
  • 3. Walter M. van den Bergh, Irene van der Schaaf, Jan van Gijn. The spectrum of presentations of venous infarction caused by deep cerebral vein thrombosis. (2005) Neurology. 65 (2): 192. <a href="https://doi.org/10.1212/01.wnl.0000179677.84785.63">doi:10.1212/01.wnl.0000179677.84785.63</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/16043785">Pubmed</a> <span class="ref_v4"></span>
  • 4. Poon CS, Chang JK, Swarnkar A, Johnson MH, Wasenko J. Radiologic diagnosis of cerebral venous thrombosis: pictorial review. (2007) AJR. American journal of roentgenology. 189 (6 Suppl): S64-75. <a href="https://doi.org/10.2214/AJR.07.7015">doi:10.2214/AJR.07.7015</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/18029905">Pubmed</a> <span class="ref_v4"></span>
  • 5. Fuentes B, Martínez-Sánchez P, Raya PG, Abenza MJ, Tejedor ED. Cerebral venous sinus thrombosis associated with cerebral hemorrhage: is anticoagulant treatment safe?. (2011) The neurologist. 17 (4): 208-10. <a href="https://doi.org/10.1097/NRL.0b013e31821a259b">doi:10.1097/NRL.0b013e31821a259b</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/21712666">Pubmed</a> <span class="ref_v4"></span>
  • 6. Coutinho J, de Bruijn SF, Deveber G, Stam J. Anticoagulation for cerebral venous sinus thrombosis. (2011) The Cochrane database of systematic reviews. <a href="https://doi.org/10.1002/14651858.CD002005.pub2">doi:10.1002/14651858.CD002005.pub2</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/21833941">Pubmed</a> <span class="ref_v4"></span>
  • 7. Ferro JM, Canhão P. Cerebral venous sinus thrombosis: update on diagnosis and management. Current cardiology reports. 16 (9): 523. <a href="https://doi.org/10.1007/s11886-014-0523-2">doi:10.1007/s11886-014-0523-2</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/25073867">Pubmed</a> <span class="ref_v4"></span>
  • 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. <a href="http://www.ncbi.nlm.nih.gov/pubmed/2272013">Pubmed citation</a><div class="ref_v2"></div>
  • 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. <a href="http://www.ajnr.org/cgi/content/full/22/3/450">AJNR Am J Neuroradiol (full text)</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/11237965">Pubmed citation</a><div class="ref_v2"></div>
  • 1. 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. <a href="http://www.ajnr.org/cgi/content/full/22/3/450">AJNR Am J Neuroradiol (full text)</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/11237965">Pubmed citation</a><div class="ref_v2"></div>
  • 2. 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. <a href="http://www.ncbi.nlm.nih.gov/pubmed/2272013">Pubmed citation</a><div class="ref_v2"></div>
  • 3. Ferro JM, Canhão P. Cerebral venous sinus thrombosis: update on diagnosis and management. Current cardiology reports. 16 (9): 523. <a href="https://doi.org/10.1007/s11886-014-0523-2">doi:10.1007/s11886-014-0523-2</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/25073867">Pubmed</a> <span class="ref_v4"></span>

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