Severity of Leukoaraiosis and Susceptibility to Infarct Growth in Acute Stroke

Ay, Hakan; Arsava, Ethem Murat; Rosand, Jonathan; Furie, Karen L.; Singhal, Aneesh B.; Schaefer, Pamela W.; Wu, Ona; González, Ramón; Koroshetz, Walter J.; Sorensen, A. Gregory

doi:10.1161/strokeaha.107.501932

Cited by 154 publications

(131 citation statements)

References 49 publications

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“…The image acquisition parameters were summarized in detail elsewhere. 24 For each imaging feature, we calculated interexaminer reliability based on assessment of 200 consecutive patients by 2 examiners blinded to each other's assignments.…”

Section: Methods Patient Population the Primary Derivationmentioning

confidence: 99%

A score to predict early risk of recurrence after ischemic stroke

Ay¹,

Güngör²,

Arsava³

et al. 2010

Neurology

129

125

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Section: Methods Patient Population the Primary Derivationmentioning

confidence: 99%

A score to predict early risk of recurrence after ischemic stroke

Ay¹,

Güngör²,

Arsava³

et al. 2010

Neurology

129

125

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“…MRI was performed by 1.5 T GE Signa (GE Medical Systems, Milwaukee, WI) or Siemens Sonata (Siemens Medical Solutions, Erlangen, Germany) scanners using the image acquisition and processing protocols that have been summarized in detail previously. 19 Acute ischemic lesion volume on DWI and leukoaraiosis volume on fluidattenuated inversion recovery (FLAIR) images acquired within 24 hours of symptom onset were determined using semiautomated region of interest outlining and volume calculation tools on the MRIcro software (www.mricro.com, University of Nottingham, UK). 9 DWI and leukoaraiosis volume measurements were performed by investigators blinded to the clinical status (TSI or ischemic stroke).…”

Section: Methods Patient Populationmentioning

confidence: 99%

Severity of leukoaraiosis determines clinical phenotype after brain infarction

Arsava¹,

Bayrlee²,

Vangel³

et al. 2011

Neurology

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Objective: To determine whether the extent of leukoaraiosis, a composite marker of baseline brain integrity, differed between patients with TIA with diffusion-weighted imaging (DWI) evidence of infarction (transient symptoms with infarction [TSI]) and patients with ischemic stroke.Methods: Leukoaraiosis volume on MRI was quantified in a consecutive series of 153 TSI and 354 ischemic stroke patients with comparable infarct volumes on DWI. We explored the relationship between leukoaraiosis volume and clinical phenotype (TIA or ischemic stroke) using a logistic regression model. Results:Patients with TSI tended to be younger (median age 66 vs 69 years, p ϭ 0.062) and had smaller median normalized leukoaraiosis volume (1.2 mL, interquartile range [IQR] 0.2-4.7 mL vs 3.5 mL, IQR 1.2-8.6 mL, p Ͻ 0.001). In multivariable analysis controlling for age, stroke risk factors, etiologic stroke mechanism, infarct volume, and infarct location, increasing leukoaraiosis volume remained associated with ischemic stroke (odds ratio 1.05 per mL, 95% confidence interval 1.02-1.09, p ϭ 0.004), along with infarct volume and infarct location. Conclusion:The probability of ischemic stroke rather than TSI increases with increasing leukoaraiosis volume, independent of infarct size and location. Our findings support the concept that the integrity of white matter tracts connecting different parts of the brain could contribute to whether or not patients develop TSI or ischemic stroke in an event of brain infarction. Neurology Approximately one-third of traditionally defined TIAs present with imaging evidence consistent with acute infarction (now termed transient symptoms with infarction [TSI]).1 Rapid and complete clinical recovery in TSI suggests that the brain has the ability to quickly compensate for the neurologic dysfunction caused by underlying infarcts. One of the most characteristic features of TSI-related infarcts is that they are invariably very small 2 ; 96% of all infarcts in TSI are smaller than 1 mL. While small infarcts are frequent in TSI, they are not specific; such small infarcts also occur in patients with clinical deficits lasting for more than 24 hours (traditionally defined ischemic stroke).2 Furthermore, small infarcts in TSI do not occur solely in so-called silent brain regions but can also involve the same brain structures that are often infarcted in ischemic stroke.2 Hence, it is not known how neurologic symptoms rapidly recover in some patients, but do not in others, despite the evidence of cerebral infarction of similar size and in similar location.Functional recovery after brain injury is a complex process which involves recruitment and reorganization of structures that are functionally similar but anatomically distinct from those that are infarcted. [3][4][5] Prior observations suggest that the integrity of the white matter as quanti-*These authors contributed equally to this work.From the A.A.

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“…21 Indeed, we and others have previously shown that leukoaraiosis severity is associated with a larger ischemic core, mismatch lost, and final infarct volume, supporting this hypothesis. 13,15,22 Indeed, subgroup analyses in patients with available follow-up imaging indicated that worse leukoaraiosis independently predicted larger infarct volumes. However, because infarct volumes could not be measured in all patients, additional studies are required to confirm the association among leukoaraiosis, infarct volume, and outcome.…”

Section: Multivariable Logistic Regression Analysis Of Factors Indepementioning

confidence: 99%