From the Departments of Radiology (M.-L.W., M.-M.Y., X.-E.W., W.-B.L.).
Neurosurgery (D.-X.Y., Y.-L.L.), Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
AJNR Am J Neuroradiol. 2018 Sep;39(9):1650-1656. doi: 10.3174/ajnr.A5737. Epub 2018 Jul 26.
Traumatic brain injury is a major public health problem worldwide. Accurately evaluating the brain microstructural changes in traumatic brain injury is crucial for the treatment and prognosis assessment. This study aimed to assess the longitudinal brain microstructural changes in traumatic brain injury in the rat using diffusional kurtosis imaging.
Diffusional kurtosis imaging was performed in a group of 5 rats at preinjury and 3, 14, and 28 days after traumatic brain injury. The diffusional kurtosis imaging parameters were measured in the bilateral cortex, hippocampus, and corpus callosum. Another 4 groups of 5 rats were used in brain immunohistochemistry analysis of neuron (neuron-specific nuclear protein [NeuN]), astroglia (glial fibrillary acidic protein [GFAP]), microglia (ionized calcium binding adaptor molecule 1 [Iba-1]), and myelin (myelin basic protein [MBP]) in the same area as the diffusional kurtosis imaging parameter measurements. Furthermore, 2 groups of 6 rats underwent a Morris water maze test at 28 days after traumatic brain injury. The diffusional kurtosis imaging parameters, immunohistochemistry results, and Morris water maze test results were compared longitudinally or between traumatic brain injury and control groups.
Compared with baseline, traumatic brain injury in the rat showed higher mean kurtosis and mean diffusivity values in the ipsilateral perilesional cortex and hippocampus and lower fractional anisotropy values in the corpus callosum ( < .05). The traumatic brain injury group showed higher staining of GFAP and Iba-1 and lower immunohistochemistry staining of NeuN and MBP in all ipsilateral ROIs ( < .05). There was no significant difference in the contralateral ROIs in diffusional kurtosis imaging parameters or immunohistochemistry results. The Morris water maze test revealed lower platform crossing times in the probe test ( < .05).
Our study indicated that there were longitudinal changes in diffusional kurtosis imaging parameters, accompanied by multiple pathologic changes at different time points following traumatic brain injury, and that mean kurtosis is more sensitive to detect microstructural changes, especially in gray matter, than mean diffusivity and fractional anisotropy.
创伤性脑损伤是全球范围内的一个主要公共卫生问题。准确评估创伤性脑损伤的脑微观结构变化对于治疗和预后评估至关重要。本研究旨在使用扩散峰度成像评估创伤性脑损伤大鼠的纵向脑微观结构变化。
在一组 5 只大鼠中，在创伤前以及创伤后 3、14 和 28 天进行扩散峰度成像。在双侧皮质、海马和胼胝体中测量扩散峰度成像参数。另外 4 组 5 只大鼠用于测量相同区域的神经元（神经元特异性核蛋白[NeuN]）、星形胶质细胞（胶质纤维酸性蛋白[GFAP]）、小胶质细胞（钙结合接头蛋白 1[Iba-1]）和少突胶质细胞（髓鞘碱性蛋白[MBP]）的免疫组织化学分析。此外，在创伤后 28 天，两组 6 只大鼠进行了 Morris 水迷宫测试。对扩散峰度成像参数、免疫组织化学结果和 Morris 水迷宫测试结果进行纵向比较或创伤性脑损伤组与对照组之间的比较。
与基线相比，大鼠创伤性脑损伤表现为对侧皮质和海马的同侧损伤区的平均峰度和平均弥散度值升高，胼胝体的各向异性分数值降低（<0.05）。创伤性脑损伤组在所有同侧 ROI 中的 GFAP 和 Iba-1 染色增加，而 NeuN 和 MBP 的免疫组织化学染色减少（<0.05）。在对侧 ROI 中，扩散峰度成像参数和免疫组织化学结果无显著差异。Morris 水迷宫测试显示，在探测测试中平台穿越次数减少（<0.05）。
我们的研究表明，在创伤性脑损伤后不同时间点存在扩散峰度成像参数的纵向变化，伴有多种病理变化，平均峰度比平均弥散度和各向异性分数更敏感地检测微观结构变化，尤其是在灰质中。
