Chiang Chia-Wen, Wang Yong, Sun Peng, Lin Tsen-Hsuan, Trinkaus Kathryn, Cross Anne H, Song Sheng-Kwei
Department of Chemistry, Washington University, St. Louis, MO 63130, USA.
Department of Radiology, Washington University School of Medicine, St. Louis, MO 63110, USA; Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA.
Neuroimage. 2014 Nov 1;101:310-9. doi: 10.1016/j.neuroimage.2014.06.064. Epub 2014 Jul 11.
The effect of extra-fiber structural and pathological components confounding diffusion tensor imaging (DTI) computation was quantitatively investigated using data generated by both Monte-Carlo simulations and tissue phantoms. Increased extent of vasogenic edema, by addition of various amount of gel to fixed normal mouse trigeminal nerves or by increasing non-restricted isotropic diffusion tensor components in Monte-Carlo simulations, significantly decreased fractional anisotropy (FA) and increased radial diffusivity, while less significantly increased axial diffusivity derived by DTI. Increased cellularity, mimicked by graded increase of the restricted isotropic diffusion tensor component in Monte-Carlo simulations, significantly decreased FA and axial diffusivity with limited impact on radial diffusivity derived by DTI. The MC simulation and tissue phantom data were also analyzed by the recently developed diffusion basis spectrum imaging (DBSI) to simultaneously distinguish and quantify the axon/myelin integrity and extra-fiber diffusion components. Results showed that increased cellularity or vasogenic edema did not affect the DBSI-derived fiber FA, axial or radial diffusivity. Importantly, the extent of extra-fiber cellularity and edema estimated by DBSI correlated with experimentally added gel and Monte-Carlo simulations. We also examined the feasibility of applying 25-direction diffusion encoding scheme for DBSI analysis on coherent white matter tracts. Results from both phantom experiments and simulations suggested that the 25-direction diffusion scheme provided comparable DBSI estimation of both fiber diffusion parameters and extra-fiber cellularity/edema extent as those by 99-direction scheme. An in vivo 25-direction DBSI analysis was performed on experimental autoimmune encephalomyelitis (EAE, an animal model of human multiple sclerosis) optic nerve as an example to examine the validity of derived DBSI parameters with post-imaging immunohistochemistry verification. Results support that in vivo DBSI using 25-direction diffusion scheme correctly reflect the underlying axonal injury, demyelination, and inflammation of optic nerves in EAE mice.
利用蒙特卡罗模拟和组织模型生成的数据，定量研究了纤维外结构和病理成分对扩散张量成像（DTI）计算的干扰作用。通过向固定的正常小鼠三叉神经添加不同量的凝胶，或在蒙特卡罗模拟中增加非受限各向同性扩散张量成分，增加血管源性水肿的程度，显著降低了分数各向异性（FA）并增加了径向扩散率，而DTI得出的轴向扩散率增加幅度较小。通过在蒙特卡罗模拟中分级增加受限各向同性扩散张量成分来模拟细胞增多，显著降低了FA和轴向扩散率，而对DTI得出的径向扩散率影响有限。还通过最近开发的扩散基谱成像（DBSI）对蒙特卡罗模拟和组织模型数据进行了分析，以同时区分和量化轴突/髓鞘完整性及纤维外扩散成分。结果表明，细胞增多或血管源性水肿并未影响DBSI得出的纤维FA、轴向或径向扩散率。重要的是，DBSI估计的纤维外细胞增多和水肿程度与实验添加的凝胶及蒙特卡罗模拟相关。我们还研究了将25方向扩散编码方案应用于相干白质束的DBSI分析的可行性。模型实验和模拟结果均表明，25方向扩散方案在纤维扩散参数及纤维外细胞增多/水肿程度的DBSI估计方面，与99方向方案相当。以实验性自身免疫性脑脊髓炎（EAE，人类多发性硬化症的动物模型）视神经为例，进行了体内25方向DBSI分析，以通过成像后免疫组织化学验证来检验得出的DBSI参数的有效性。结果支持，使用25方向扩散方案的体内DBSI能够正确反映EAE小鼠视神经潜在的轴突损伤、脱髓鞘和炎症情况。
