Cavitation After Acute Symptomatic Lacunar Stroke Depends on Time, Location, and MRI Sequence

Moreau, F.; Patel, Shiel K.; Lauzon, M. Louis; McCreary, Cheryl R.; Goyal, Mayank; Frayne, Richard; Demchuk, Andrew M.; Coutts, Shelagh B.; Smith, Eric E.

doi:10.1161/strokeaha.111.647859

Cited by 86 publications

(89 citation statements)

References 30 publications

(30 reference statements)

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“…The long‐term appearance of the symptomatic small subcortical infarcts varies: up to 10% disappear completely, between 30 and 95% cavitate to form a lacune, and the rest retain an appearance identical to a WMH (Loos, Staals, Wardlaw, & van Oostenbrugge, 2012; Moreau et al., 2012; Potter et al., 2010). Some other features like cortical microinfarcts and tissue changes in the normal‐appearing white matter cannot be identified on standard MRI (Gouw et al., 2011) at 1.5T.…”

Section: Discussionmentioning

confidence: 99%

Interhemispheric characterization of small vessel disease imaging markers after subcortical infarct

et al. 2016

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BackgroundIn structural Magnetic Resonance Imaging (MRI) of patients with a recent small subcortical infarct (RSSI) and small vessel disease (SVD) imaging markers coexist. However, their spatial distribution and prevalence with respect to the hemisphere of the RSSI remain unknown.Materials and MethodsFrom brain MRI in 187 patients with an acute lacunar ischemic stroke clinical syndrome and a relevant diffusion weighted imaging (DWI)‐positive lesion, we semiautomatically extracted the RSSI, microbleeds, lacunes, old cortical infarcts, and white matter hyperintensities (WMH) using optimized thresholding in the relevant sequences, and rated the load of perivascular spaces. We registered all images to an age‐relevant brain template and calculated the probability distribution of all SVD markers mentioned for patients who had the RSSI in each hemisphere separately. We used the Wilcoxon and chi‐squared tests to compare the volumes and frequencies of occurrence, respectively, of the SVD markers between hemispheres throughout the sample.ResultsFifty‐two percent patients (n = 97) had the RSSI in the left hemisphere, 42% (n = 78) in the right, 2.7% (n = 5) in both, and 3.7% (n = 7) in the cerebellum or brainstem. There was no significant difference in RSSI frequency between left and right hemispheres (p = .10) in the sample. The median volume of the RSSI (expressed as a percentage of the total intracranial volume) was 0.05% (IQR = 0.06). There was no difference in median percent volume of the right RSSIs versus left (p = .16). Neither was there a significant interhemispheric difference in the volume of any of the SVD markers regardless of the location of the RSSI and they were equally distributed in both hemispheres.ConclusionAssessment of SVD imaging markers in the contralateral hemisphere could be used as a proxy for the SVD load in the whole brain to avoid contamination by the RSSI of the measurements, especially of WMH.

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Section: Discussionmentioning

confidence: 99%

Interhemispheric characterization of small vessel disease imaging markers after subcortical infarct

et al. 2016

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“…Infarcts identified on diffusionweighted images can have different appearances on follow-up imaging, ranging from cavitation (complete tissue loss) to normal-appearing. [16][17][18] To assess the relationship between different imaging appearances on follow-up examinations and changes within the connected cortex or the affected tracts, infarcts were classified into 3 groups using the T1-weighted and fluid-attenuated inversion recovery (FLAIR) images at follow-up: (1) cavitating (parts of the infarct turned into a cavity), (2) noncavitating (no cavitation, parts of the infarct turned into a FLAIR hyperintensity), and (3) no visible T1 or FLAIR lesion at the site of the original infarct.…”

Section: Methods Study Cohortmentioning

confidence: 99%

Acute infarcts cause focal thinning in remote cortex via degeneration of connecting fiber tracts

et al. 2015

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Objective: To study remote effects distant from acute ischemic infarcts by measuring longitudinal changes of cortical thickness in connected brain regions as well as changes in microstructural integrity in connecting fiber tracts.Methods: Thirty-two patients (mean age 71 years) underwent a standardized protocol including multimodal MRI and clinical assessment both at stroke onset and 6 months after the event. Cortex connected to acute infarcts was identified by probabilistic diffusion tensor tractography starting from the acute lesion. Changes of cortical thickness were measured using the longitudinal stream of FreeSurfer. Microstructural damage in white matter tracts was assessed by changes of mean diffusivity. Results:We found focal cortical thinning specifically in areas connected to acute infarcts (p , 0.001). Thinning was more pronounced in regions showing a high probability of connectivity to infarcts. Microstructural damage in white matter tracts connecting acute infarcts with distant cortex significantly correlated with thickness changes in that region (r 5 20.39, p 5 0.028). There was no indication of an influence of cavitation status or infarct etiology on the observed changes in cortex and white matter.Conclusions: These findings identify secondary degeneration of connected white matter tracts and remote cortex as key features of acute ischemic infarcts. Our observations may have implications for the understanding of structural and functional reorganization after stroke. Remote cortical effects of acute infarcts critically contribute to functional reorganization after stroke and influence clinical outcome.1,2 We recently identified focal cortical thinning as a potential structural correlate of remote effects after ischemic lesions. In a small retrospective study on 9 patients with inherited small vessel disease, we showed that incident subcortical lacunes are associated with focal thinning in cortex connected to the infarct. 3,4 We attributed these findings to secondary cortical neurodegeneration following damage to the connecting subcortical fiber tracts. However, the study protocol and small sample size precluded a detailed assessment of these tracts and how changes in these tracts relate to changes in the connected cortex. Also, the results were obtained in a rare hereditary condition and were limited to a single infarct mechanism and to chronic, cavitating infarcts.In the current prospective, longitudinal study, we investigated the processes driving secondary neurodegeneration after acute infarcts. We measured changes of cortical thickness and microstructural integrity of connecting white matter tracts over a 6-month interval starting from stroke onset. We tested the following hypotheses: (1) cortical thinning in connected cortical regions is detectable within a few months after an acute infarct; (2) cortical thinning relates to *These authors contributed equally to this work.

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“…They usually, but not always, exhibit central hypointensity on the FLAIR sequence, often with an irregular rim of T2 hyperintensity reflecting adjacent gliosis; however, sometimes they appear hyperintense on FLAIR as a result of incomplete suppression of the intracavitary fluid ( Figure 3). 26 On CT, they appear as areas of hypodensity with attenuation similar to that of cerebrospinal fluid (Figure 2). They are differentiated from perivascular spaces by size (≥3 mm), shape (ovoid and irregular instead of linear or sausage-shaped), and location.…”

Section: Silent Brain Infarctsmentioning

confidence: 99%

“…However, longitudinal studies show that some acute lacunar infarcts do not develop cavitation and therefore will be misclassified as WMHs in their chronic phase. 26,28 Additionally, although the size criterion of ≥3 mm is useful to increase the specificity for infarction as opposed to perivascular space, neuropathological studies frequently identify much smaller infarcts, called microinfarcts, that are unapparent on routine clinical imaging. 29,30 Therefore, MRI is likely to substantially underestimate the burden of infarction in some patients.…”

Section: Silent Brain Infarctsmentioning

confidence: 99%

Prevention of Stroke in Patients With Silent Cerebrovascular Disease: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

Smith¹,

Saposnik²,

Biessels³

et al. 2017

Stroke

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Abstract-Two decades of epidemiological research shows that silent cerebrovascular disease is common and is associated with future risk for stroke and dementia. It is the most common incidental finding on brain scans. To summarize evidence on the diagnosis and management of silent cerebrovascular disease to prevent stroke, the Stroke Council of the American Heart Association convened a writing committee to evaluate existing evidence, to discuss clinical considerations, and to offer suggestions for future research on stroke prevention in patients with 3 cardinal manifestations of silent cerebrovascular disease: silent brain infarcts, magnetic resonance imaging white matter hyperintensities of presumed vascular origin, and cerebral microbleeds. The writing committee found strong evidence that silent cerebrovascular disease is a common problem of aging and that silent brain infarcts and white matter hyperintensities are associated with future symptomatic stroke risk independently of other vascular risk factors. In patients with cerebral microbleeds, there was evidence of a modestly increased risk of symptomatic intracranial hemorrhage in patients treated with thrombolysis for acute ischemic stroke but little prospective evidence on the risk of symptomatic hemorrhage in patients on anticoagulation. There were no randomized controlled trials targeted specifically to participants with silent cerebrovascular disease to prevent stroke. Primary stroke prevention is indicated in patients with silent brain infarcts, white matter hyperintensities, or microbleeds. Adoption of standard terms and definitions for silent cerebrovascular disease, as provided by prior American Heart Association/American Stroke Association statements and by a consensus group, may facilitate diagnosis and communication of findings from radiologists to clinicians. (Stroke. 2017;48:e44-e71.

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Cavitation After Acute Symptomatic Lacunar Stroke Depends on Time, Location, and MRI Sequence

Cited by 86 publications

References 30 publications

Interhemispheric characterization of small vessel disease imaging markers after subcortical infarct

Interhemispheric characterization of small vessel disease imaging markers after subcortical infarct

Acute infarcts cause focal thinning in remote cortex via degeneration of connecting fiber tracts

Prevention of Stroke in Patients With Silent Cerebrovascular Disease: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

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