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| Diffusion tensor imaging analysis of crossed cerebellar diaschisis after cerebral infarction in rats |
| LIN Ya-nan, CHENG Jing-liang, ZHANG Yong, YANG Lu, ZHAO Shan-shan, ZHANG Xiao-nan |
| The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450000, China |
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Abstract Objective: To detect the change of diffusion parameter in remote regions of the infarct core after middle cerebral artery occlusion(MACO) in rats using diffusion tensor imaging(DTI), to detect the RGMa protein expression of the brain tissue by immunohistochemistry, and to detect the diffusion and pathological changes of the cerebral infarction core area and bilateral cerebellar hemispheres, and to further understand the relevant mechanism of crossed cerebellar diaschisis(CCD). Methods: All the animals were randomly divided into experimental group(n=56) and control group(n=14). After making the successful model, the control group and the experimental group rats underwent MRI at 1 h, 3 h, 6 h, 9 h, 12 h, 24 h and 72 h, and the expression of RGMa protein was detected by immunohistochemistry in the bilateral cerebellar hemispheres of rats. Results: The results of MRI in the experimental group at each time point after MCAO in rats showed that the FA values were all decreased in the bilateral cerebellar hemisphere compared with normal control group, and the FA values were decreased to the lowest at 12 h, and the FA value of the contralateral(right) cerebellar hemisphere was significantly lower than that of the ipsilateral(left) cerebellar hemisphere. The results of immunohistochemistry showed that the expressions of RGMa protein were increased in the bilateral cerebellar hemisphere compared with the normal control group, and the expression were increased to the peak at 24 h, and the expression of the contralateral cerebellar hemisphere was significantly higher than that of the ipsilateral cerebellar hemisphere. Conclusion: The MR DTI combined with RGMa protein pathology can be used to detect the phenomenon of CCD after supratentorial cerebral infarction, and to explain the mechanism of CCD.
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Received: 23 June 2016
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