Not All Lesioned Tissue Is Equal: Identifying Pericavitational Areas in Chronic Stroke With Tissue Integrity Gradation via T2w T1w Ratio.

Not All Lesioned Tissue Is Equal: Identifying Pericavitational Areas in Chronic Stroke With Tissue Integrity Gradation via T2w T1w Ratio.
复制标题

DOI:
10.3389/fnins.2021.665707
复制
发表时间:
2021
影响因子:
4.3
通讯作者:
Crosson BA
Crosson BA
中科院分区:
医学2区
文献类型:
--
作者:
Krishnamurthy LC;Krishnamurthy V;Rodriguez AD;McGregor KM;Glassman CN;Champion GS;Rocha N;Harnish SM;Belagaje SR;Kundu S;Crosson BA

文献摘要

参考文献

被引文献

相似文献

脑损伤区域内的中风相关组织损伤在拓扑学上是不均匀的,并且具有潜在的组织组成变化,这可能对康复具有重要意义。然而,我们知道没有统一接受的,客观的非侵入性的方法来确定慢性中风病变内的腔周区域。为了填补这一空白,我们提出了一种新的磁共振成像(MRI)方法,客观地量化病变核心和周围的围腔周长,我们称之为组织完整性分级通过T2w T1w比(TIGR)。TIGR使用在临床环境中常规收集的标准T1加权(T1w)和T2加权(T2w)解剖图像。分析TIGR图与受试者特定的灰质和脑脊液阈值的关系,并进行分箱,以创建中风病变内组织损伤的假彩色图,并将其进一步分类为低损伤、中损伤和高损伤区域。我们通过显示病变内的脑血流量随着组织损伤的增加而减少来验证TIGR(p = 0.005)。我们进一步表明,一个显着的任务活动,可以检测到在腔周区,中度损伤区包含一个显着较低的幅度的血流动力学反应功能比相邻的受损区域(p < 0.0001)。我们还证明了使用TIGR图提取多变量脑行为关系的可行性(p < 0.05),并显示与二元病变、仅T1w和仅T2w图相比,位置大致一致,但脑行为图的范围可能取决于稀疏系数(p < 0.0001)表示的信号灵敏度。最后,我们展示了在早期和晚期亚急性卒中阶段量化TIGR的可行性,其中较高损伤区域的尺寸较小(p = 0.002),并且随着卒中后时间的增加,受损体素从较低损伤过渡到较高损伤(p = 0.004)。我们得出结论,TIGR能够(1)在不同的卒中后时间点识别卒中病变内的组织损伤梯度,以及(2)更客观地从腔周区域描绘病变核心,其中这些区域表现出合理和预期的生理和功能障碍。重要的是,由于T1w和T2w扫描是在诊所中常规收集的,因此TIGR图可以很容易地结合到临床环境中,而无需额外的成像成本或患者负担,以促进与康复计划相关的决策过程。
Stroke-related tissue damage within lesioned brain areas is topologically non-uniform and has underlying tissue composition changes that may have important implications for rehabilitation. However, we know of no uniformly accepted, objective non-invasive methodology to identify pericavitational areas within the chronic stroke lesion. To fill this gap, we propose a novel magnetic resonance imaging (MRI) methodology to objectively quantify the lesion core and surrounding pericavitational perimeter, which we call tissue integrity gradation via T2w T1w ratio (TIGR). TIGR uses standard T1-weighted (T1w) and T2-weighted (T2w) anatomical images routinely collected in the clinical setting. TIGR maps are analyzed with relation to subject-specific gray matter and cerebrospinal fluid thresholds and binned to create a false colormap of tissue damage within the stroke lesion, and these are further categorized into low-, medium-, and high-damage areas. We validate TIGR by showing that the cerebral blood flow within the lesion reduces with greater tissue damage (p = 0.005). We further show that a significant task activity can be detected in pericavitational areas and that medium-damage areas contain a significantly lower magnitude of hemodynamic response function than the adjacent damaged areas (p < 0.0001). We also demonstrate the feasibility of using TIGR maps to extract multivariate brain–behavior relationships (p < 0.05) and show general agreement in location compared to binary lesion, T1w-only, and T2w-only maps but that the extent of brain behavior maps may depend on signal sensitivity as denoted by the sparseness coefficient (p < 0.0001). Finally, we show the feasibility of quantifying TIGR in early and late subacute stroke phases, where higher-damage areas were smaller in size (p = 0.002) and that lesioned voxels transition from lower to higher damage with increasing time post-stroke (p = 0.004). We conclude that TIGR is able to (1) identify tissue damage gradient within the stroke lesion across different post-stroke timepoints and (2) more objectively delineate lesion core from pericavitational areas wherein such areas demonstrate reasonable and expected physiological and functional impairments. Importantly, because T1w and T2w scans are routinely collected in the clinic, TIGR maps can be readily incorporated in clinical settings without additional imaging costs or patient burden to facilitate decision processes related to rehabilitation planning.
DOI: 10.1016/j.neuron.2015.02.027
发表时间: 2015-03-04
期刊: Neuron
影响因子: 16.2
作者:
Corbetta M;Ramsey L;Callejas A;Baldassarre A;Hacker CD;Siegel JS;Astafiev SV;Rengachary J;Zinn K;Lang CE;Connor LT;Fucetola R;Strube M;Carter AR;Shulman GL
通讯作者: Shulman GL
DOI: 10.1016/j.neuron.2013.12.034
发表时间: 2014-01-22
期刊: Neuron
影响因子: 16.2
作者:
Burda JE;Sofroniew MV
通讯作者: Sofroniew MV
DOI: 10.1007/bf02985612
发表时间: 2004-02-01
影响因子: 2.6
作者:
Ibaraki, M;Shimosegawa, E;Hatazawa, J
通讯作者: Hatazawa, J
DOI: 10.1136/jnnp.2007.132100
发表时间: 2008-06-01
影响因子: 11
作者:
Bang, O. Y.;Saver, J. L.;Liebeskind, D. S.
通讯作者: Liebeskind, D. S.
DOI: 10.1038/jcbfm.2013.77
发表时间: 2013-08-01
影响因子: 6.3
作者:
Campbell, Bruce C. V.;Christensen, Soren;Davis, Stephen M.
通讯作者: Davis, Stephen M.