Lacunar infarct
Updates to Article Attributes
Lacunar infarcts are small (<20;15 mm) infarcts in the distal distribution of deep penetrating vessels (lenticulostriate, thalamoperforating, and pontine perforating arteries, recurrent artery of Heubner). They result from occlusion of one of the small penetrating end arteries at the base of the brain and are due to fibrinoid degeneration.
Clinical presentation
Patients without diagnostic imaging whoMost lacunar infarcts are clinically silent, but repeated episodes are associated with vascular dementia. Symptomatic patients may present with symptoms of a lacunar stroke may be described as suffering from a lacunar stroke syndrome (LACS), one of five distinct syndromes.
Pathology
They areLacunar infarcts, by definition, are caused by occlusion of one of the small penetrating end-arteries at the base of the brain,and must be smaller than 15 mm. They are thought to result primarily from in situ microatheroma formation, or lipohyalinosis 2 (c.f. cortical infarcts where embolisation of distal thrombus is the primary aetiology).
Pathologically, they are small holes of encephalomalacia and are traversed by a cob-web-like mesh of fibrous strands.
Radiographic features
CT /
In an acute setting, lacunar infarcts appear as ill-defined hypodensities.
Chronic lesions appear as hypodense foci (similar to CSF).
MRI
In an acute setting, the following signal changes are seen:
-
small discrete foci of hypodensity /diffusion restriction - T2/FLAIR: hyperintense
-
DWI: restricted diffusion
- may demonstrate acute lesions not visible on other sequences
3-20 mm in diameter, most commonly 10 mm-
T1C+:may enhance
in the lateif acuteor(or early subacutestage unilateral pontine infarcts have a sharp demarcation at the midline-
higher signal intensity than CSF (marginalgliosis)
Chronic lesions are isointense to CSF on all sequences but may demonstrate a peripheral T2/FLAIR hyperintense rim of marginal gliosis.
History and etymology
The term was penned by Charles Miller Fisher, a Canadian neurologist, who described "lacunes" (Latin: lake) of empty fluid within the brains of stroke victims post mortem-mortem.
Differential diagnosis
-<p><strong>Lacunar infarcts</strong> are small (<20 mm) infarcts in the distal distribution of deep penetrating vessels (<a href="/articles/lenticulostriate-arteries">lenticulostriate</a>, thalamoperforating, and <a href="/articles/pontine-perforating-arteries">pontine perforating arteries</a>, <a href="/articles/recurrent-artery-of-huebner">recurrent artery of Heubner</a>). They result from occlusion of one of the small penetrating end arteries at the base of the brain and are due to fibrinoid degeneration.</p><h4>Clinical presentation</h4><p>Patients without diagnostic imaging who present with symptoms of a lacunar stroke may be described as suffering from a <a href="/articles/lacunar-stroke-syndrome">lacunar stroke syndrome (LACS)</a>, one of five distinct syndromes.</p><h4>Pathology</h4><p>They are caused by occlusion of one of the small penetrating end-arteries at the base of the brain, thought to result primarily from in situ microatheroma formation, or lipohyalinosis <sup>2</sup> (c.f. cortical infarcts where embolisation of distal thrombus is the primary aetiology).</p><p>Pathologically, they are small holes of <a href="/articles/encephalomalacia">encephalomalacia</a> and are traversed by a cob-web-like mesh of fibrous strands.</p><h4>Radiographic features</h4><h5>CT / MRI</h5><ul>-<li>small discrete foci of hypodensity / <a href="/articles/diffusion-weighted-mri-in-acute-stroke-1">diffusion restriction</a>- +<p><strong>Lacunar infarcts</strong> are small (<15 mm) infarcts in the distal distribution of deep penetrating vessels (<a href="/articles/lenticulostriate-arteries">lenticulostriate</a>, thalamoperforating, and <a href="/articles/pontine-perforating-arteries">pontine perforating arteries</a>, <a href="/articles/recurrent-artery-of-huebner">recurrent artery of Heubner</a>). They result from occlusion of one of the small penetrating end arteries at the base of the brain and are due to fibrinoid degeneration.</p><h4>Clinical presentation</h4><p>Most lacunar infarcts are clinically silent, but repeated episodes are associated with <a href="/articles/vascular-dementia">vascular dementia</a>. Symptomatic patients may present with <a href="/articles/lacunar-stroke-syndrome">lacunar stroke syndrome (LACS)</a>, one of five distinct syndromes.</p><h4>Pathology</h4><p>Lacunar infarcts, by definition, are caused by occlusion small penetrating end-arteries and must be smaller than 15 mm. They are thought to result primarily from in situ microatheroma formation or <a href="/articles/lipohyalinosis">lipohyalinosis</a> <sup>2</sup>.</p><p>Pathologically, they are small holes of <a href="/articles/encephalomalacia">encephalomalacia</a> and are traversed by a cob-web-like mesh of fibrous strands.</p><h4>Radiographic features</h4><h5>CT</h5><p>In an acute setting, lacunar infarcts appear as ill-defined hypodensities.</p><p>Chronic lesions appear as hypodense foci (similar to CSF).</p><h5>MRI</h5><p>In an acute setting, the following signal changes are seen:</p><ul>
- +<li>
- +<strong>T1:</strong> slightly hypointense</li>
- +<li>
- +<strong>T2/FLAIR:</strong> hyperintense</li>
- +<li>
- +<strong>DWI: </strong>restricted diffusion<ul><li>may demonstrate acute lesions not visible on other sequences</li></ul>
-<li>3-20 mm in diameter, most commonly 10 mm</li>-<li>may enhance in the late acute or early subacute stage</li>-<li>unilateral pontine infarcts have a sharp demarcation at the midline</li>-<li>higher signal intensity than CSF (marginal <a href="/articles/gliosis">gliosis</a>)</li>-</ul><h4>History and etymology</h4><p>The term was penned by <strong>Charles Miller Fisher</strong>, a Canadian neurologist who described "lacunes" (Latin: <em>lake</em>) of empty fluid within the brains of stroke victims post mortem.</p><h4>Differential diagnosis</h4><ul>- +<li>
- +<strong>T1C+:</strong> may enhance if acute (or early subacute)</li>
- +</ul><p>Chronic lesions are isointense to CSF on all sequences but may demonstrate a peripheral T2/FLAIR hyperintense rim of marginal <a title="Gliosis" href="/articles/gliosis">gliosis</a>.</p><h4>History and etymology</h4><p>The term was penned by <strong>Charles Miller Fisher</strong>, a Canadian neurologist, who described "lacunes" (Latin: <em>lake</em>) of empty fluid within the brains of stroke victims post-mortem.</p><h4>Differential diagnosis</h4><ul>
- +<li><a title="Ischaemic stroke" href="/articles/ischaemic-stroke">embolic stroke</a></li>
-<li><a title="Striatocapsular infarct" href="/articles/striatocapsular-infarct">striatocapsular infarct</a></li>- +<li><a href="/articles/striatocapsular-infarct">striatocapsular infarct</a></li>