Cerebral edema

Changed by Jeremy Jones, 3 Apr 2023
Back to revision history
Disclosures - updated 6 Dec 2022: Nothing to disclose

Updates to Article Attributes

Body was changed:

Cerebral oedema refers to a number of interconnected processes which result in abnormal shifts of water across various compartments of the brain parenchyma. It is observed in the majority of injuries involving the central nervous system 5.

It has traditionally been broadly divided into vasogenic cerebral oedema and cytotoxic cerebral oedema, the latter a term commonly used to denote both true cytotoxic oedema and ionic oedema 4. In addition, although traditionally not included in discussions on oedema, haemorrhagic transformation can be thought of as an extreme end-stage form of the same processes which lead to oedema. 

As such, a more precise classification is 3,4:

Special types of oedema to be considered: 

Treatment and prognosis

Promising drugs for the pharmacological treatment of cerebral oedema, in any clinical trial phase, include (but are not limited to) 5:

  • conivaptan (dual, a dual antagonist of AVParginine vasopressin (AVP) V1A and V2 receptors)

  • fingolimod (sphingosine, a sphingosine-1-phosphate receptor modulator)

  • celecoxib (COX, a COX-2 inhibitor)

  • glyburide (antidiabetic, an antidiabetic sulfonylurea)

  • human corticotropin-releasing factor (hCRF)

  • bevacizumab (humanized, a humanized monoclonal VEGF-A inhibiting antibody)

  • cediranib (potent, a potent pan-VEGF RTK inhibitor)

  • -<p><strong>Cerebral oedema</strong> refers to a number of interconnected processes which result in abnormal shifts of water across various compartments of the brain parenchyma. It is observed in the majority of injuries involving the <a href="/articles/central-nervous-system-1" title="Central nervous system">central nervous system</a> <sup>5</sup>.</p><p>It has traditionally been broadly divided into <a href="/articles/vasogenic-cerebral-oedema">vasogenic cerebral oedema</a> and <a href="/articles/cytotoxic-cerebral-oedema">cytotoxic cerebral oedema</a>, the latter a term commonly used to denote both true cytotoxic oedema and ionic oedema <sup>4</sup>. In addition, although traditionally not included in discussions on oedema, haemorrhagic transformation can be thought of as an extreme end-stage form of the same processes which lead to oedema. </p><p>As such a more precise classification is <sup>3,4</sup>:</p><ul>
  • -<li>
  • -<p><a href="/articles/cytotoxic-cerebral-oedema">cytotoxic cerebral oedema</a></p>
  • -<ul><li><p><a href="/articles/ionic-cerebral-oedema">ionic cerebral oedema</a> </p></li></ul>
  • -</li>
  • -<li><p><a href="/articles/vasogenic-cerebral-oedema">vasogenic cerebral oedema</a></p></li>
  • -<li><p>osmotic cerebral oedema</p></li>
  • -</ul><p>Special types of oedema to be considered: </p><ul>
  • -<li><p><a href="/articles/transependymal-oedema">transependymal oedema</a> (also known as interstitial cerebral oedema)</p></li>
  • -<li><p><a href="/articles/combined-cerebral-oedema">combined cerebral oedema</a></p></li>
  • -</ul><h4>Treatment and prognosis</h4><p>Promising drugs for the pharmacological treatment of cerebral oedema, in any clinical trial phase, include (but are not limited to) <sup>5</sup>:</p><ul>
  • -<li><p>conivaptan (dual antagonist of AVP V<sub>1</sub>A and V<sub>2</sub> receptors)</p></li>
  • -<li><p>fingolimod (sphingosine-1-phosphate receptor modulator)</p></li>
  • -<li><p>celecoxib (COX-2 inhibitor)</p></li>
  • -<li><p>glyburide (antidiabetic sulfonylurea)</p></li>
  • -<li><p>human corticotropin-releasing factor (hCRF)</p></li>
  • -<li><p>bevacizumab (humanized monoclonal VEGF-A inhibiting antibody)</p></li>
  • -<li><p>cediranib (potent pan-VEGF RTK inhibitor)</p></li>
  • +<p><strong>Cerebral oedema</strong> refers to a number of interconnected processes which result in abnormal shifts of water across various compartments of the brain parenchyma. It is observed in the majority of injuries involving the <a href="/articles/central-nervous-system-1" title="Central nervous system">central nervous system</a> <sup>5</sup>.</p><p>It has traditionally been broadly divided into <a href="/articles/vasogenic-cerebral-oedema">vasogenic cerebral oedema</a> and <a href="/articles/cytotoxic-cerebral-oedema">cytotoxic cerebral oedema</a>, the latter a term commonly used to denote both true cytotoxic oedema and ionic oedema <sup>4</sup>. In addition, although traditionally not included in discussions on oedema, haemorrhagic transformation can be thought of as an extreme end-stage form of the same processes which lead to oedema. </p><p>As such, a more precise classification is <sup>3,4</sup>:</p><ul>
  • +<li>
  • +<p><a href="/articles/cytotoxic-cerebral-oedema">cytotoxic cerebral oedema</a></p>
  • +<ul><li><p><a href="/articles/ionic-cerebral-oedema">ionic cerebral oedema</a> </p></li></ul>
  • +</li>
  • +<li><p><a href="/articles/vasogenic-cerebral-oedema">vasogenic cerebral oedema</a></p></li>
  • +<li><p><a href="/articles/osmotic-cerebral-oedema" title="osmotic cerebral oedema">osmotic cerebral oedema</a></p></li>
  • +</ul><p>Special types of oedema to be considered: </p><ul>
  • +<li><p><a href="/articles/transependymal-oedema">transependymal oedema</a> (also known as interstitial cerebral oedema)</p></li>
  • +<li><p><a href="/articles/combined-cerebral-oedema">combined cerebral oedema</a></p></li>
  • +</ul><h4>Treatment and prognosis</h4><p>Promising drugs for the pharmacological treatment of cerebral oedema in any clinical trial phase, include (but are not limited to) <sup>5</sup>:</p><ul>
  • +<li><p>conivaptan, a dual antagonist of arginine vasopressin (AVP) V<sub>1</sub>A and V<sub>2</sub> receptors</p></li>
  • +<li><p>fingolimod, a sphingosine-1-phosphate receptor modulator</p></li>
  • +<li><p>celecoxib, a COX-2 inhibitor</p></li>
  • +<li><p>glyburide, an antidiabetic sulfonylurea</p></li>
  • +<li><p>human corticotropin-releasing factor (hCRF)</p></li>
  • +<li><p>bevacizumab, a humanized monoclonal VEGF-A inhibiting antibody</p></li>
  • +<li><p>cediranib, a potent pan-VEGF RTK inhibitor</p></li>

References changed:

  • 1. Na D, Kim E, Ryoo J et al. CT Sign of Brain Swelling Without Concomitant Parenchymal Hypoattenuation: Comparison with Diffusion- and Perfusion-Weighted MR Imaging. Radiology. 2005;235(3):992-48. <a href="https://doi.org/10.1148/radiol.2353040571">doi:10.1148/radiol.2353040571</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/15860675">Pubmed</a>
  • 2. Wijdicks E, Plevak D, Rakela J, Wiesner R. Clinical and Radiologic Features of Cerebral Edema in Fulminant Hepatic Failure. Mayo Clin Proc. 1995;70(2):119-24. <a href="https://doi.org/10.4065/70.2.119">doi:10.4065/70.2.119</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/7845036">Pubmed</a>
  • 3. Ho M, Rojas R, Eisenberg R. Cerebral Edema. AJR Am J Roentgenol. 2012;199(3):W258-73. <a href="https://doi.org/10.2214/AJR.11.8081">doi:10.2214/AJR.11.8081</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/22915416">Pubmed</a>
  • 4. Simard J, Kent T, Chen M, Tarasov K, Gerzanich V. Brain Oedema in Focal Ischaemia: Molecular Pathophysiology and Theoretical Implications. Lancet Neurol. 2007;6(3):258-68. <a href="https://doi.org/10.1016/S1474-4422(07)70055-8">doi:10.1016/S1474-4422(07)70055-8</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/17303532">Pubmed</a>
  • 1. Na DG, Kim EY, Ryoo JW et-al. CT sign of brain swelling without concomitant parenchymal hypoattenuation: comparison with diffusion- and perfusion-weighted MR imaging. Radiology. 2005;235 (3): 992-48. <a href="http://dx.doi.org/10.1148/radiol.2353040571">doi:10.1148/radiol.2353040571</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/15860675">Pubmed citation</a><div class="ref_v2"></div>
  • 2. Wijdicks EF, Plevak DJ, Rakela J et-al. Clinical and radiologic features of cerebral edema in fulminant hepatic failure. Mayo Clin. Proc. 1995;70 (2): 119-24. <a href="http://dx.doi.org/10.1016/S0025-6196(11)64278-X">doi:10.1016/S0025-6196(11)64278-X</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/7845036">Pubmed citation</a><div class="ref_v2"></div>
  • 3. Ho ML, Rojas R, Eisenberg RL. Cerebral edema. AJR Am J Roentgenol. 2012;199 (3): W258-73. <a href="http://dx.doi.org/10.2214/AJR.11.8081">doi:10.2214/AJR.11.8081</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/22915416">Pubmed citation</a><span class="ref_v3"></span>
  • 4. Simard JM, Kent TA, Chen M et-al. Brain oedema in focal ischaemia: molecular pathophysiology and theoretical implications. Lancet Neurol. 2007;6 (3): 258-68. <a href="http://dx.doi.org/10.1016/S1474-4422(07)70055-8">doi:10.1016/S1474-4422(07)70055-8</a> - <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725365">Free text at pubmed</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/17303532">Pubmed citation</a><span class="auto"></span>

ADVERTISEMENT: Supporters see fewer/no ads