Abstract

Lacunar infarct has been characterized as small subcortical infarct. It is postulated to occur from "in situ microatheroma or lipohyalinosis" in small vessel or lacunar mechanism. Based on this idea, such infarcts by lacunar mechanism should not be associated with large area of perfusion deficits that extend beyond the subcortical region to the cortical region. By contrast, selected small subcortical infarcts, as defined by MR imaging in the subacute and chronic stage, may initially have large perfusion deficit or related large vessel occlusions. These infarcts with "lacunar" phenotype may also be caused by disease in the parent vessel and may have very different stroke mechanism from small vessel disease. Our aim is to describe differences in imaging characteristics between patients with small subcortical infarction with "lacunar phenotype" from those with lacunar mechanism. Patients undergoing acute CT perfusion/angiography (CTP/CTA) within 6 h of symptom onset and follow-up magnetic resonance imaging (MRI) for ischemic stroke were included (2009-2013). Lacunar infarct was defined as a single subcortical infarct ≤20 mm on follow-up MRI. Presence of perfusion deficits, vessel occlusion, and infarct dimensions was compared between lacunar infarcts and other topographical infarct types. Overall, 182 patients (mean age 66.4 ± 15.3 years, 66% males) were included. Lacunar infarct occurred in 31 (17%) patients. Of these, 12 (39%) patients had a perfusion deficit compared with those with any cortical infarction (120/142, 67%), and the smallest lacunar infarct with a perfusion deficit had a diameter of <5 mm. The majority of patients with lacunar infarction (8/12, 66.7%) had a relevant vessel occlusion. A quarter of lacunar infarcts had a large artery stroke mechanism evident on acute CTP/CTA. Lacunar mechanism was present in 3/8 patients with corona radiata, 5/10 lentiform nucleus, 5/6 posterior limb of internal capsule (PLIC), 3/5 thalamic infarcts, 1/2 miscellaneous locations. There was a trend to significant with regards to finding lacunar mechanism among patients with thalamic and PLIC infarcts versus lentiform nucleus and corona radiata infarcts (p = 0.13). Diverse stroke mechanisms were present among subcortical infarcts in different locations. When available acute CTP/CTA should be combined with subacute imaging of subcortical infarct to separate "lacunar phenotype" from those with lacunar mechanism.

Highlights

  • Lacunar infarct accounts for up to 20% of acute ischemic strokes [1]

  • Patients with ischemic stroke admitted to the stroke unit at the Monash Medical Centre, Melbourne, Australia, between April 2009 and March 2013 were retrospectively selected through a search of the hospital radiology databases and included if acute CT perfusion (CTP)/CT angiography (CTA) and follow-up magnetic resonance imaging (MRI) were conducted

  • From group A to group E, we found a significant increase in proportions with cardioembolic stroke mechanism (p for trend = 0.043) and a significant decrease in proportions with undetermined stroke mechanism (p for trend < 0.001)

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Summary

Introduction

Lacunar infarct accounts for up to 20% of acute ischemic strokes [1]. This infarct is identified based on its subcortical locations using MR imaging. Fisher had listed the location by frequencies as lentiform, caudate, thalamus, pons, posterior limb of internal capsule (PLIC), and convolutional white matter [2] They have been postulated to occur from “in situ microatheroma or lipohyalinosis” [3] in small cerebral vessels such as penetrating arteries [2] in the territories of the recurrent artery of Heubner (RAH), lenticulostriate (LA), anterior and posterior choroidal, thalamoperforating, thalamogeniculate, or pontine paramedian arteries [4]. By contrast, selected small subcortical infarcts, as defined by MR imaging in the subacute and chronic stage, may initially have large perfusion deficit or related large vessel occlusions These infarcts with “lacunar” phenotype may be caused by disease in the parent vessel and may have very different stroke mechanism from small vessel disease. Our aim is to describe differences in imaging characteristics between patients with small subcortical infarction with “lacunar phenotype” from those with lacunar mechanism

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