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

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

DOI:
10.1161/01.str.31.12.3008
复制
发表时间:
2000-12-01
期刊:
影响因子:
8.3
通讯作者:
Warlow, CP
Warlow, CP
中科院分区:
医学1区
文献类型:
--
作者:
Wild, JM;Wardlaw, JM;Warlow, CP

文献摘要

被引文献

相似文献

背景和目的:通常认为在T2 MRI上显示异常的组织已经梗死,任何半暗影位于T2可见病变之外。我们利用磁共振质子光谱研究梗死组织的分布。方法:在有急性半球缺血性脑卒中症状的患者中,在脑卒中后最多3天内成像,我们利用质子磁共振成像(proton spectral MRI)在t2加权MR图像上异常(高强度)区域内和周围探测n -乙酰天冬氨酸(NAA)的分布,这是一种完整神经元的标志物。结果:在II型患者中,在中风发作后24至72小时成像,除了T2图像上的高强度边缘外,几乎没有证据表明神经元受损(NAA减少)。而在T2异常区域内,T2明显异常区(非常高)与轻度异常区(轻微高)的NAA数量(即完整神经元的比例)差异有统计学意义。结论t2可见病变的高强度范围和程度直接反映神经元的损伤程度;没有t2可见病变提示在成像时主要是完整的神经元。我们假设,一旦组织损伤达到临界(可能是不可逆的)水平,T2图像迅速变得异常,在梗死的病理分期和T2显示之间没有明显的时间滞后。需要在更大的研究中进一步测试血流量水平来证实这一点。
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, imaged 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 abnormal (hyperintense) areas on T2-weighted MR images, using proton spectroscopic 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 hyperintensity on the T2 image. However, within the abnormal T2 area, there were statistically significant differences in the amount of NAA (ie, the proportion of intact neurons) between areas that were obviously abnormal on T2 (very hyperintense) and those that were only slightly abnormal (slightly hyperintense).Conclusions-The extent and degree of hyperintensity of the T2-visible lesion directly reflect the amount of neuronal damage; lack of a T2-visible lesion would suggest predominantly intact neurons at the time of imaging. We hypothesize that once tissue damage has reached a critical (probably irreversible) level, the T2 image quickly becomes abnormal without any significant time lag between the pathological staging of the infarct and its visualization on T2. Further testing in a larger study with information on blood flow levels would be required to confirm this.