Watershed cerebral infarction
Updates to Article Attributes
Watershed cerebral infarctions, also known as border zone infarcts, occur at the border between cerebral vascular territories with no or little anastomosis where the tissue is furthest from arterial supply and thus most vulnerable to reductions in perfusion.
Epidemiology
TheyWatershed cerebral infarction account for 5-10% of all cerebral infarctions 8. They tend to be seen in the elderly, who have a higher incidence of arterial stenosis and hypotensive episodes, as well as microemboli.
Pathology
It has been proposed that both, episodes of hypoperfusion and microembolisms from inflammed atherosclerotic plaques, play a role in pathophysiology of this entity. Clearance of, although the microemboli are most likely to be impaired in watershed zones due to poorer perfusionlater is less well established 5.
Episodes of systemic hypotension alongparticularly with severe stenosis or occlusion of the feeding arteries, in particular intra and extracranial carotid arteries can also contribute, is the typical scenario in which watershed infarction is encountered.
Clearance of the microemboli, which may form on the surface of inflamed plaques, or are the result of an embolic shower, are most likely to the infarctionbe impaired in watershed zones due to poorer perfusion.
Watershed zone infarct in an isolated zonearea is more likely to be secondary to microembolism, particularly in the absence of significant systemic hypotension and/or arterial stenosis. In a severe carotid stenosis, lesions are usually unilateral on the side ofipsilateral to the stenosis. Prolonged hypotension such as cardiac surgery or cardiac arrest commonly give a bilateral pattern in the absence of sever stenosis 5.
WSIWatershed infarction has been classified to:
-
cortical (external) border zones infarct
- between ACA, MCA, and PCA territories
-
mostly due to microembolihistologically these can be wedges of cortical and subcortical infarction, or cortical laminar necrosis
-
deep (internal) border zones infarct:
- between ACA, MCA, and PCA territories, and perforating medullary, lenticulostriate, recurrent artery of Heubner and anterior choroidal arteries
mostly due to either severe hypotension or severe arterial stenosis
Radiographic features
CT and MRI
Exact pattern depends on the bordering territories which is usually variable in different individuals. Imaging of WSIwatershed infarction should also aim to determine presence and severity of arterial stenosis or occlusion.
Cortical (external) border zones infarct
These are usually wedge-shaped or gyriform:
- ACA/MCA: in frontal cortex extending from anterior horn to the cortex
- MCA/PCA: in parieto-occipital region extending from posterior horn to the cortex
- parallel parafalcine stripes in subcortical white matter at the vertex- this type is seen when there was profound diffuse hypoperfusion
Triple watershed zone: most vulnerable region where ACA, MCA, and PCA converge posterior to lateral ventricles in parieto-occipital region.
Deep (internal) border zones infarct
- ≥3 lesions, each ≥3 mm in diameter in a linear fashion parallel to the lateral ventricles in the centrum semiovale or corona radiata, which sometimes become more confluent and band-like 7
Differential diagnosis
-<p><strong>Watershed cerebral infarctions</strong>, also known as <strong>border zone infarcts</strong>, occur at the border between <a href="/articles/cerebral-vascular-territories">cerebral vascular territories</a> with no or little anastomosis. </p><h4>Epidemiology</h4><p>They account for 5-10% of all cerebral infarctions <sup>8</sup>. </p><h4>Pathology</h4><p>It has been proposed that both, episodes of hypoperfusion and microembolisms, play a role in pathophysiology of this entity. Clearance of the microemboli are most likely to be impaired in watershed zones due to poorer perfusion. Episodes of systemic hypotension along with severe stenosis or occlusion of the feeding arteries, in particular intra and extracranial carotid arteries can also contribute to the infarction. </p><p>Watershed zone infarct in an isolated zone is more likely to be secondary to microembolism in the absence of significant systemic hypotension. In a severe <a href="/articles/carotid-stenosis">carotid stenosis</a> lesions are usually unilateral on the side of the stenosis. Prolonged hypotension such as cardiac surgery or cardiac arrest commonly give a bilateral pattern <sup>5</sup>. </p><p>WSI has been classified to:</p><ul>- +<p><strong>Watershed cerebral infarctions</strong>, also known as <strong>border zone infarcts</strong>, occur at the border between <a href="/articles/cerebral-vascular-territories">cerebral vascular territories</a> where the tissue is furthest from arterial supply and thus most vulnerable to reductions in perfusion. </p><h4>Epidemiology</h4><p>Watershed cerebral infarction account for 5-10% of all <a href="/articles/ischaemic-stroke">cerebral infarctions</a> <sup>8</sup>. They tend to be seen in the elderly, who have a higher incidence of arterial stenosis and hypotensive episodes, as well as microemboli. </p><h4>Pathology</h4><p>It has been proposed that both, episodes of hypoperfusion and microembolisms from inflammed atherosclerotic plaques, play a role in pathophysiology of this entity, although the later is less well established <sup>5</sup>.</p><p>Episodes of systemic hypotension particularly with severe stenosis or occlusion of the feeding arteries, in particular intra and extracranial carotid arteries, is the typical scenario in which watershed infarction is encountered. </p><p>Clearance of the microemboli, which may form on the surface of inflamed plaques, or are the result of an embolic shower, are most likely to be impaired in watershed zones due to poorer perfusion. </p><p>Watershed zone infarct in an isolated area is more likely to be secondary to microembolism, particularly in the absence of significant systemic hypotension and/or arterial stenosis. In a severe <a href="/articles/carotid-stenosis">carotid stenosis</a>, lesions are usually ipsilateral to the stenosis. Prolonged hypotension such as cardiac surgery or cardiac arrest commonly give a bilateral pattern in the absence of sever stenosis <sup>5</sup>. </p><p>Watershed infarction has been classified to:</p><ul>
-<li>mostly due to microemboli</li>- +<li>histologically these can be wedges of cortical and subcortical infarction, or <a href="/articles/cortical-laminar-necrosis">cortical laminar necrosis</a>
- +</li>
-<strong>deep (internal)</strong> border zones infarct: <ul>-<li>between ACA, MCA, and PCA territories, and perforating medullary, lenticulostriate, recurrent artery of Heubner and anterior choroidal arteries</li>-<li>mostly due to either severe hypotension or severe arterial stenosis</li>-</ul>- +<strong>deep (internal)</strong> border zones infarct: <ul><li>between ACA, MCA, and PCA territories, and perforating medullary, lenticulostriate, <a href="/articles/recurrent-artery-of-heubner-1">recurrent artery of Heubner</a> and anterior choroidal arteries</li></ul>
-</ul><h4>Radiographic features</h4><h6>CT and MRI</h6><p>Exact pattern depends on the bordering territories which is usually variable in different individuals. Imaging of WSI should also aim to determine presence and severity of arterial stenosis or occlusion.</p><h5>Cortical (external) border zones infarct</h5><p>These are usually wedge-shaped or gyriform:</p><ul>- +</ul><h4>Radiographic features</h4><h5>CT and MRI</h5><p>Exact pattern depends on the bordering territories which is usually variable in different individuals. Imaging of watershed infarction should also aim to determine presence and severity of arterial stenosis or occlusion.</p><h6>Cortical (external) border zones infarct</h6><p>These are usually wedge-shaped or gyriform:</p><ul>
-</ul><p>Triple watershed zone: most vulnerable region where ACA, MCA, and PCA converge posterior to lateral ventricles in parieto-occipital region.</p><h5>Deep (internal) border zones infarct</h5><ul><li>≥3 lesions, each ≥3 mm in diameter in a linear fashion parallel to the lateral ventricles in the <a href="/articles/centrum-semiovale-1">centrum semiovale</a> or <a href="/articles/corona-radiata">corona radiata</a>, which sometimes become more confluent and band-like <sup>7</sup>-</li></ul><h4>Differential diagnosis</h4><ul>-<li><a href="/articles/embolic-infarcts">embolic infarcts</a></li>-<li><a href="/articles/posterior-reversible-encephalopathy-syndrome-1">PRES</a></li>-<li><a href="/articles/lacunar-infarct">lacunar infarcts</a></li>-</ul>- +</ul><p>Triple watershed zone: most vulnerable region where ACA, MCA, and PCA converge posterior to lateral ventricles in parieto-occipital region.</p><h6>Deep (internal) border zones infarct</h6><ul><li>≥3 lesions, each ≥3 mm in diameter in a linear fashion parallel to the lateral ventricles in the <a href="/articles/centrum-semiovale-1">centrum semiovale</a> or <a href="/articles/corona-radiata">corona radiata</a>, which sometimes become more confluent and band-like <sup>7</sup>
- +</li></ul>
References changed:
- 9. Vinay Kumar, Abul K. Abbas, Jon C. Aster. Robbins and Cotran Pathologic Basis of Disease, Professional Edition E-Book. (2014) ISBN: 9780323296359 - <a href="http://books.google.com/books?vid=ISBN9780323296359">Google Books</a>
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