N-acetylaspartate distribution in proton spectroscopic images of ischemic stroke - Relationship to infarct appearance on T2-weighted magnetic resonance imaging

Citation
Jm. Wild et al., N-acetylaspartate distribution in proton spectroscopic images of ischemic stroke - Relationship to infarct appearance on T2-weighted magnetic resonance imaging, STROKE, 31(12), 2000, pp. 3008-3014
Citations number
37
Categorie Soggetti
Neurology,"Cardiovascular & Hematology Research
Journal title
STROKE
ISSN journal
00392499 → ACNP
Volume
31
Issue
12
Year of publication
2000
Pages
3008 - 3014
Database
ISI
SICI code
0039-2499(200012)31:12<3008:NDIPSI>2.0.ZU;2-3
Abstract
Background and Purpose-It is generally considered that tissue that appears abnormal on T2 MRI is already infarcted and that any penumbra lies outside the T2-visible lesion. We investigated the distribution of infarcted tissue using proton spectroscopic MRI. Methods-In patients with symptoms of acute hemispheric ischemic stroke, ima ged within a maximum of 3 days of stroke, we explored the distribution of N -acetylaspartate (NAA), a marker of intact neurons, within and around the a bnormal (hyperintense) areas on T2-weighted MR images, using proton spectro scopic MRI. Results-In II patients, imaged 24 to 72 hours after stroke onset, there was little evidence of damaged neurons (reduced NAA) beyond the margins of hyp erintensity on the T2 image. However, within the abnormal T2 area, there we re statistically significant differences in the amount of NAA (ie, the prop ortion of intact neurons) between areas that were obviously abnormal on T2 (very hyperintense) and those that were only slightly abnormal (slightly hy perintense). Conclusions-The extent and degree of hyperintensity of the T2-visible lesio n directly reflect the amount of neuronal damage; lack of a T2-visible lesi on would suggest predominantly intact neurons at the time of imaging. We hy pothesize that once tissue damage has reached a critical (probably irrevers ible) level, the T2 image quickly becomes abnormal without any significant time lag between the pathological staging of the infarct and its visualizat ion on T2. Further testing in a larger study with information on blood flow levels would be required to confirm this.