Characterizing physiological heterogeneity of infarction risk in acute human ischaemic stroke using MRI.

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Characterizing physiological heterogeneity of infarction risk in acute human ischaemic stroke using MRI. / Wu, Ona; Christensen, Søren; Hjort, Niels; Dijkhuizen, Rick M; Kucinski, Thomas; Fiehler, Jens; Thomalla, Götz; Röther, Joachim; Østergaard, Leif.

In: BRAIN, Vol. 129, No. 9, 9, 2006, p. 2384-2393.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Wu, O, Christensen, S, Hjort, N, Dijkhuizen, RM, Kucinski, T, Fiehler, J, Thomalla, G, Röther, J & Østergaard, L 2006, 'Characterizing physiological heterogeneity of infarction risk in acute human ischaemic stroke using MRI.', BRAIN, vol. 129, no. 9, 9, pp. 2384-2393. <http://www.ncbi.nlm.nih.gov/pubmed/16891322?dopt=Citation>

APA

Wu, O., Christensen, S., Hjort, N., Dijkhuizen, R. M., Kucinski, T., Fiehler, J., Thomalla, G., Röther, J., & Østergaard, L. (2006). Characterizing physiological heterogeneity of infarction risk in acute human ischaemic stroke using MRI. BRAIN, 129(9), 2384-2393. [9]. http://www.ncbi.nlm.nih.gov/pubmed/16891322?dopt=Citation

Vancouver

Wu O, Christensen S, Hjort N, Dijkhuizen RM, Kucinski T, Fiehler J et al. Characterizing physiological heterogeneity of infarction risk in acute human ischaemic stroke using MRI. BRAIN. 2006;129(9):2384-2393. 9.

Bibtex

@article{2b3d26c4ebaf41ebb526398391546846,
title = "Characterizing physiological heterogeneity of infarction risk in acute human ischaemic stroke using MRI.",
abstract = "Viable tissues at risk of infarction in acute stroke patients have been hypothesized to be detectable as volumetric mismatches between lesions on perfusion-weighted (PWI) and diffusion-weighted magnetic resonance imaging (DWI). Because tissue response to ischaemic injury and to therapeutic intervention is tissue- and patient-dependent, changes in infarct progression due to treatment may be better detected with voxel-based methods than with volumetric mismatches. Acute DWI and PWI were combined using a generalized linear model (GLM) to predict infarction risk on a voxel-wise basis for patients treated either with non-thrombolytic (Group 1; n = 11) or with thrombolytic therapy (Group 2; n = 27). Predicted infarction risk for both groups was evaluated in four ipsilateral regions of interest: tissue acutely abnormal on DWI (Core), tissue acutely abnormal on PWI but normal on DWI that either infarcts (Recruited) or does not (Salvaged), and tissue normal on both DWI and PWI that does not infarct (Normal) by follow-up imaging > or = 5 days. The performance of the models was significantly reduced for the thrombolysed group compared with the group receiving standard treatment, suggesting an alteration in natural progression of the ischaemic cascade. Average GLM-predicted infarction risk values in the four regions were different from one another for both groups. GLM-predicted infarction risk in Salvaged tissue was significantly higher (P = 0.02) for thrombolysed patients than for non-thrombolysed patients, suggesting that thrombolysis rescued tissue with higher infarction risk than typically measured in tissue that spontaneously recovered. The observed spatial heterogeneity of GLM-predicted infarction risk values probably reflects the varying degrees of tissue injury and salvageability that exist after stroke. MRI-based algorithms may therefore provide a more sensitive means for monitoring therapeutic effects on a voxel-wise basis.",
author = "Ona Wu and S{\o}ren Christensen and Niels Hjort and Dijkhuizen, {Rick M} and Thomas Kucinski and Jens Fiehler and G{\"o}tz Thomalla and Joachim R{\"o}ther and Leif {\O}stergaard",
year = "2006",
language = "Deutsch",
volume = "129",
pages = "2384--2393",
journal = "BRAIN",
issn = "0006-8950",
publisher = "Oxford University Press",
number = "9",

}

RIS

TY - JOUR

T1 - Characterizing physiological heterogeneity of infarction risk in acute human ischaemic stroke using MRI.

AU - Wu, Ona

AU - Christensen, Søren

AU - Hjort, Niels

AU - Dijkhuizen, Rick M

AU - Kucinski, Thomas

AU - Fiehler, Jens

AU - Thomalla, Götz

AU - Röther, Joachim

AU - Østergaard, Leif

PY - 2006

Y1 - 2006

N2 - Viable tissues at risk of infarction in acute stroke patients have been hypothesized to be detectable as volumetric mismatches between lesions on perfusion-weighted (PWI) and diffusion-weighted magnetic resonance imaging (DWI). Because tissue response to ischaemic injury and to therapeutic intervention is tissue- and patient-dependent, changes in infarct progression due to treatment may be better detected with voxel-based methods than with volumetric mismatches. Acute DWI and PWI were combined using a generalized linear model (GLM) to predict infarction risk on a voxel-wise basis for patients treated either with non-thrombolytic (Group 1; n = 11) or with thrombolytic therapy (Group 2; n = 27). Predicted infarction risk for both groups was evaluated in four ipsilateral regions of interest: tissue acutely abnormal on DWI (Core), tissue acutely abnormal on PWI but normal on DWI that either infarcts (Recruited) or does not (Salvaged), and tissue normal on both DWI and PWI that does not infarct (Normal) by follow-up imaging > or = 5 days. The performance of the models was significantly reduced for the thrombolysed group compared with the group receiving standard treatment, suggesting an alteration in natural progression of the ischaemic cascade. Average GLM-predicted infarction risk values in the four regions were different from one another for both groups. GLM-predicted infarction risk in Salvaged tissue was significantly higher (P = 0.02) for thrombolysed patients than for non-thrombolysed patients, suggesting that thrombolysis rescued tissue with higher infarction risk than typically measured in tissue that spontaneously recovered. The observed spatial heterogeneity of GLM-predicted infarction risk values probably reflects the varying degrees of tissue injury and salvageability that exist after stroke. MRI-based algorithms may therefore provide a more sensitive means for monitoring therapeutic effects on a voxel-wise basis.

AB - Viable tissues at risk of infarction in acute stroke patients have been hypothesized to be detectable as volumetric mismatches between lesions on perfusion-weighted (PWI) and diffusion-weighted magnetic resonance imaging (DWI). Because tissue response to ischaemic injury and to therapeutic intervention is tissue- and patient-dependent, changes in infarct progression due to treatment may be better detected with voxel-based methods than with volumetric mismatches. Acute DWI and PWI were combined using a generalized linear model (GLM) to predict infarction risk on a voxel-wise basis for patients treated either with non-thrombolytic (Group 1; n = 11) or with thrombolytic therapy (Group 2; n = 27). Predicted infarction risk for both groups was evaluated in four ipsilateral regions of interest: tissue acutely abnormal on DWI (Core), tissue acutely abnormal on PWI but normal on DWI that either infarcts (Recruited) or does not (Salvaged), and tissue normal on both DWI and PWI that does not infarct (Normal) by follow-up imaging > or = 5 days. The performance of the models was significantly reduced for the thrombolysed group compared with the group receiving standard treatment, suggesting an alteration in natural progression of the ischaemic cascade. Average GLM-predicted infarction risk values in the four regions were different from one another for both groups. GLM-predicted infarction risk in Salvaged tissue was significantly higher (P = 0.02) for thrombolysed patients than for non-thrombolysed patients, suggesting that thrombolysis rescued tissue with higher infarction risk than typically measured in tissue that spontaneously recovered. The observed spatial heterogeneity of GLM-predicted infarction risk values probably reflects the varying degrees of tissue injury and salvageability that exist after stroke. MRI-based algorithms may therefore provide a more sensitive means for monitoring therapeutic effects on a voxel-wise basis.

M3 - SCORING: Zeitschriftenaufsatz

VL - 129

SP - 2384

EP - 2393

JO - BRAIN

JF - BRAIN

SN - 0006-8950

IS - 9

M1 - 9

ER -