Elevated T2-values in MRI of stroke patients shortly after symptom onset do not predict irreversible tissue infarction

Distinct from signal alterations in diffusion-weighted images, T(2)-values are also dependent on tissue water content and known to increase with time from symptom onset in acute ischaemic stroke. The purpose of this study was to evaluate whether there is a detectable increase of T(2)-values in diffe...

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Published inBrain (London, England : 1878) Vol. 135; no. Pt 6; pp. 1981 - 1989
Main Authors SIEMONSEN, Susanne, LÖBEL, Ulricke, SEDLACIK, Jan, FORKERT, Nils D, MOURIDSEN, Kim, ØSTERGAARD, Leif, THOMALLA, Gotz, FIEHLER, Jens
Format Journal Article
LanguageEnglish
Published Oxford Oxford University Press 01.06.2012
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Summary:Distinct from signal alterations in diffusion-weighted images, T(2)-values are also dependent on tissue water content and known to increase with time from symptom onset in acute ischaemic stroke. The purpose of this study was to evaluate whether there is a detectable increase of T(2)-values in different regions in acute ischaemic stroke in the acute and subacute situation and to study the effect of recanalization on the evaluation of T(2)-values in the subacute phase. In addition, we sought to evaluate whether this increase in T(2)-values is reversible. For this purpose, 22 patients with acute ischaemic stroke in the territory of the middle cerebral artery underwent magnetic resonance imaging including diffusion-weighted imaging, perfusion-weighted imaging, fluid-attenuated inversion recovery to determine final infarct size, time-of-flight-angiography (acute and on day 1 or 2) and a triple echo-T(2)-sequence (calculation of T(2) maps) within 6 h after symptom onset. Images were co-registered and regions of diffusion restriction and prolonged time-to-peak as well as surviving tissue (surviving tissue = time-to-peak - final infarct size) and lesion growth (lesion growth = final infarct size-diffusion restriction) were defined and superimposed onto the quantitative T(2) map. In addition, patients were dichotomized according to recanalization information. Mean quantitative T(2)-values were derived for each patient within each region of interest. Mean T(2)-values for patients with recanalization (n = 15) in surviving tissue region of interest were 115.8 ± 7.2 ms (mean ± SD) and in the lesion growth region of interest 114.6 ± 7.0 ms. T(2)-values for patients without recanalization (n = 7) were 117.7 ± 11.4 ms in surviving tissue region of interest and 117.3 ± 12.1 ms in lesion growth region of interest. There was no significant difference between T(2)-values measured in lesion growth and surviving tissue region of interest for patients with or without recanalization. Even though it has been shown that T(2)-values increase with time from symptom onset within the infarct core, increased T(2)-values in areas of perfusion impairment do not identify irreversible damaged brain tissue and high T(2)-values are even found in tissue that is not part of the final infarct lesion and can therefore normalize. In conclusion, this study suggests that T(2)-values are not a valid imaging biomarker in acute stroke to predict tissue outcome.
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ISSN:0006-8950
1460-2156
DOI:10.1093/brain/aws079