Watershed cerebral infarction
Updates to Article Attributes
Watershed cerebral infarctions, also known as border zone infarcts, occur at the border between cerebral vascular territories where the tissue is furthest from arterial supply and thus most vulnerable to reductions in perfusion.
Epidemiology
Watershed cerebral infarction accountaccounts for 5-10% of all cerebral infarctions 8. They tend to occur in the elderly, who have a higher incidence of arterial stenosis and hypotensive episodes, as well as sources of microemboli.
Pathology
ItAlthough traditionally watershed infarction has been proposedthought of as being due primarily to hypoperfusion, more recently there is mounting evidence that both episodes of hypoperfusion and/or microemboli from inflamed atherosclerotic plaques play a role in pathophysiology of this entity, although the latter is less well establishedor other sources can be causative 53,5.
Episodes of systemic hypotension, particularly combined with severe inflow stenosis or occlusion of the feeding arteries, in particular the intracranial and extracranial (e.g. carotid arteriesstenosis), is the typical scenario in which a watershed infarction is encountered and classically affects the deep border zone (string of pearls sign) but can also involve the external border zone 3. The location of stenoses and anatomy of the circle of Willis will contribute to the location of infarcts.
ClearanceIn contrast, clearance of the microemboli, which may form on the surface of inflamed plaques or are the result of an embolic shower (including fat embolism and air embolism11,12), are most usually only affect the external (cortical) border zone presumably as the absence of abundant collateral supply makes these areas more likely to be impaired in watershed zones due to poorer perfusioninfarct from small occlusions 103,10.
A watershedThus, in the absence of significant inflow impairment, a border 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 carotid stenosis, lesions are usually ipsilateral to the stenosis. Prolonged hypotension, such as during cardiac surgery or cardiac arrest, commonly gives a bilateral pattern in the absence of severe stenosis 5
Watershed infarction has been classified as:
-
cortical (external) border zones infarct
- due to either hypoperfusion or microemboli
- between ACA, MCA, and PCA territories
- histologically, these can be wedges of cortical and subcortical infarction or cortical laminar necrosis
-
deep (internal) border zones infarct:
- due to hypoperfusion
- between ACA, MCA, and PCA territories and perforating medullary, lenticulostriate, recurrent artery of Heubner and anterior choroidal arteries
Radiographic features
CT and MRI
The exact pattern depends on the bordering territories, which are usually variable in different individuals. Imaging of watershed infarction should also aim to determine the presence and severity of arterial stenosis and occlusion.
Cortical (external) border zones infarct
These are usually wedge-shaped or gyriform:
- ACA/MCA: in the frontal cortex, extending from the anterior horn to the cortex
- MCA/PCA: in the parieto-occipital region, extending from the posterior horn to the cortex
- parallel parafalcine stripes in the subcortical white matter at the vertex - this type is seen with profound diffuse hypoperfusion
Triple watershed zone: most vulnerable region where ACA, MCA, and PCA converge in the parieto-occipital region posterior to the lateral ventricles.
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 radiate, (string of pearls) which sometimes become more confluent and band-like 7
-<p><strong>Watershed cerebral infarctions</strong>, also known as <strong>border zone infarcts</strong>, occur at the border between <a href="/articles/brain-arterial-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 occur 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 microemboli from inflamed atherosclerotic plaques play a role in pathophysiology of this entity, although the latter 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 the intracranial and extracranial carotid arteries, is the typical scenario in which a 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 <sup>10</sup>. </p><p>A 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 during cardiac surgery or cardiac arrest, commonly gives a bilateral pattern in the absence of severe stenosis <sup>5</sup>. </p><p>Watershed infarction has been classified as:</p><ul>- +<p><strong>Watershed cerebral infarctions</strong>, also known as <strong>border zone infarcts</strong>, occur at the border between <a href="/articles/brain-arterial-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 accounts for 5-10% of all <a href="/articles/ischaemic-stroke">cerebral infarctions</a> <sup>8</sup>. They tend to occur in the elderly, who have a higher incidence of arterial stenosis and hypotensive episodes, as well as sources of microemboli. </p><h4>Pathology</h4><p>Although traditionally watershed infarction has been thought of as being due primarily to hypoperfusion, more recently there is mounting evidence that both episodes of hypoperfusion and/or microemboli from inflamed atherosclerotic plaques or other sources can be causative <sup>3,5</sup>.</p><p>Episodes of systemic hypotension, particularly combined with severe inflow stenosis or occlusion (e.g. <a href="/articles/carotid-stenosis">carotid stenosis</a>), is the typical scenario in which a watershed infarction is encountered and classically affects the deep border zone (<a title="String of pearls sign (watershed infarction)" href="/articles/string-of-pearls-sign-watershed-infarction">string of pearls sign</a>) but can also involve the external border zone <sup>3</sup>. The location of stenoses and anatomy of the circle of Willis will contribute to the location of infarcts. </p><p>In contrast, clearance of the microemboli, which may form on the surface of inflamed plaques or are the result of an embolic shower (including <a title="Cerebral fat embolism" href="/articles/cerebral-fat-embolism">fat embolism</a> and <a title="Cerebral air embolism" href="/articles/cerebral-air-embolism">air embolism</a> <sup>11,12</sup>), usually only affect the external (cortical) border zone presumably as the absence of abundant collateral supply makes these areas more likely to infarct from small occlusions <sup>3,10</sup>. </p><p>Thus, in the absence of significant inflow impairment, a border zone infarct in an isolated area is more likely to be secondary to microembolism. </p><ul>
- +<li>due to either hypoperfusion or microemboli</li>
-<strong>deep (internal)</strong> border zones infarct: <ul><li>between ACA, MCA, and PCA territories and perforating medullary, <a href="/articles/lenticulostriate-arteries">lenticulostriate</a>, <a href="/articles/recurrent-artery-of-heubner-1">recurrent artery of Heubner</a> and <a href="/articles/anterior-choroidal-artery">anterior choroidal arteries</a>-</li></ul>- +<strong>deep (internal)</strong> border zones infarct: <ul>
- +<li>due to hypoperfusion</li>
- +<li>between ACA, MCA, and PCA territories and perforating medullary, <a href="/articles/lenticulostriate-arteries">lenticulostriate</a>, <a href="/articles/recurrent-artery-of-heubner-1">recurrent artery of Heubner</a> and <a href="/articles/anterior-choroidal-artery">anterior choroidal arteries</a>
- +</li>
- +</ul>
References changed:
- 11. Dimitre Mirtchev, Tapan Mehta, Annie Daniel, Thomas Finstein, Louise McCullough. Pearls & Oy-sters: Enhancing vigilance for detection of cerebral air embolism. (2018) Neurology. 91 (15): 717. <a href="https://doi.org/10.1212/WNL.0000000000006324">doi:10.1212/WNL.0000000000006324</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/30297504">Pubmed</a> <span class="ref_v4"></span>
- 12. Ahmed ElSadek, Ahmed Gaber, Hossam Afifi, Sherin Farag, Nouran Salaheldien. Microemboli versus hypoperfusion as an etiology of acute ischemic stroke in Egyptian patients with watershed zone infarction. (2019) The Egyptian Journal of Neurology, Psychiatry and Neurosurgery. 55 (1): 1. <a href="https://doi.org/10.1186/s41983-018-0045-8">doi:10.1186/s41983-018-0045-8</a> <span class="ref_v4"></span>
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