Diffusion kurtosis as an in vivo imaging marker for reactive astrogliosis in traumatic brain injury.

Diffusion kurtosis as an in vivo imaging marker for reactive astrogliosis in traumatic brain injury.
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DOI:
10.1016/j.neuroimage.2011.07.050
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发表时间:
2012-01-02
期刊:
影响因子:
5.7
通讯作者:
Gullapalli RP
Gullapalli RP
中科院分区:
医学1区
文献类型:
--
作者:
Zhuo J;Xu S;Proctor JL;Mullins RJ;Simon JZ;Fiskum G;Gullapalli RP

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扩散峰度成像(DKI)提供了关于生物组织中水扩散的非高斯行为的可量化信息。在轻度控制性皮质撞击(CCI)损伤大鼠模型中,研究了损伤后急性(2小时)和亚急性(7天)阶段几个白色和灰质区域的水扩散张量成像(DTI)参数和DKI参数的变化。混合模型方差分析显示,在皮层,海马,外囊和胼胝体的DTI和DKI参数的时间模式的显着变化。事后检验表明双侧皮质和海马的平均扩散率(MD)(p < 0.0005)以及同侧皮质(p <0.0005)、海马(p = 0.014)、胼胝体(p = 0.031)和对侧外囊(p = 0.011)的各向异性分数(FA)发生了急性变化。这些变化在亚急性期恢复至基线水平。然而,在亚急性期,所有同侧区域的平均峰度(MK)显著升高,并与距撞击部位的距离成反比(皮质和胼胝体:p < 0.0005;外囊:p = 0.003;海马:p = 0.011)。此外,在亚急性期,与基线相比,在对侧区域也观察到MK增加(皮质:p = 0.032;海马:p = 0.039),而MD和FA未观察到变化。平均峰度的增加与免疫组化分析的反应性星形胶质细胞增生增加相关。我们的研究结果表明,DKI是敏感的反应性星形胶质细胞增生的微结构变化,可能会错过标准的DTI参数单独。监测MK的变化可以调查由于反应性星形胶质细胞增生引起的体内分子和形态学变化,并可以补充标准DTI参数提供的信息。迄今为止,扩散张量成像的应用仅限于研究创伤性损伤后白色物质完整性的变化。鉴于DKI的敏感性,以检测显微结构的变化,甚至在灰质在体内,允许扩展的技术,以了解病理形态学的变化,在整个大脑的创伤性损伤后。
Diffusion Kurtosis Imaging (DKI) provides quantifiable information on the non-Gaussian behavior of water diffusion in biological tissue. Changes in water diffusion tensor imaging (DTI) parameters and DKI parameters in several white and grey matter regions were investigated in a mild controlled cortical impact (CCI) injury rat model at both the acute (2 hours) and the sub-acute (7 days) stages following injury. Mixed model ANOVA analysis revealed significant changes in temporal patterns of both DTI and DKI parameters in the cortex, hippocampus, external capsule and corpus callosum. Post-hoc tests indicated acute changes in mean diffusivity (MD) in the bilateral cortex and hippocampus (p < 0.0005) and fractional anisotropy (FA) in ipsilateral cortex (p < 0.0005), hippocampus (p = 0.014), corpus callosum (p = 0.031) and contralateral external capsule (p = 0.011). These changes returned to baseline by the sub-acute stage. However, mean kurtosis (MK) was significantly elevated at the sub-acute stages in all ipsilateral regions and scaled inversely with the distance from the impacted site (cortex and corpus callosum: p < 0.0005; external capsule: p = 0.003; hippocampus: p = 0.011). Further, at the sub-acute stage increased MK was also observed in the contralateral regions compared to baseline (cortex: p = 0.032; hippocampus: p = 0.039) while no change was observed with MD and FA. An increase in mean kurtosis was associated with increased reactive astrogliosis from immunohistochemistry analysis. Our results suggest that DKI is sensitive to microstructural changes associated with reactive astrogliosis which may be missed by standard DTI parameters alone. Monitoring changes in MK allows the investigation of molecular and morphological changes in vivo due to reactive astrogliosis and may complement information available from standard DTI parameters. To date the use of diffusion tensor imaging has been limited to study changes in white matter integrity following traumatic insults. Given the sensitivity of DKI to detect microstructural changes even in the gray matter in vivo, allows the extension of the technique to understand patho-morphological changes in the whole brain following a traumatic insult.
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