慢性膝骨关节炎患者大脑结构形态的改变

关键词：膝骨关节炎  磁共振成像  灰质体积  脑沟深度  结构协变网络

Keywords:knee osteoarthritis  magnetic resonance imaging  gray matter volume  sulcus depth  structural covariance networks

摘要：

      摘要 目的：探索慢性膝骨关节炎患者大脑结构形态的变化特点。 方法：使用基于体素的形态学测量分析（voxel-based morphometry， VBM）和基于表面的形态学测量分析（surface-based morphometry， SBM）以及基于灰质体积构建的结构协变网络（structural covariance networks， SCN）分析慢性膝骨关节炎（knee osteoarthritis， KOA）患者大脑结构形态与健康受试者（healthy control， HC）间的差异。 结果：①VBM分析：与HC受试者相比较，慢性KOA患者以左侧颞极（temporal pole）为中心区域的灰质体积显著减小（voxels水平，P<0.001；cluster水平，P=0.049，FWE校正，voxels size=833）。②SBM分析：与HC受试者相比较，慢性KOA患者左侧额下回盖部（pars opercularis）区域脑沟深度显著减小（voxels水平，P<0.001；cluster水平，P=0.003，FWE校正，voxels size=293）。③SCN分析：与HC受试者相比较，慢性KOA患者基于局部灰质体积构建的SCN鲁棒性强于HC受试者（P=0.032）。 结论：慢性KOA患者存在大脑结构形态的异常，这为慢性KOA对中枢神经系统可能的影响提供了新的理解。

Abstract:

      Abstract Objective： To explore the characteristics of brain structure and morphology changes in patients with chronic knee osteoarthritis (OA). Method: Voxel-based morphometry（VBM） analysis， surface-based morphometry（SBM） analysis and structural covariance networks（SCN）based on gray matter volume were used to exam the differences in brain structure and morphology between patients with chronic knee osteoarthritis（KOA） and healthy control（HC）. Result： ①VBM analysis：Compared with HC subjects，chronic KOA patients showed a significant reduction in gray matter volume of the left temporal pole as the central region（voxels level，P<0.001；cluster level，P=0.049，FWE correction，voxels size=833）.②SBM analysis：Compared with HC subjects，the sulcus depth in the pars opercularis of the left inferior frontal gyrus decreased significantly in patients with chronic KOA（voxels level，P<0.001；cluster level，P=0.003，FWE correction，voxels size=293）.③SCN analysis：Compared with HC subjects，the SCN constructed based on local gray matter volume in patients with chronic KOA was more robust than that in healthy controls（P=0.032）. Conclusion： Chronic KOA patients have structural abnormalities in the brain， providing a new insights into the potential impact of chronic KOA on the central nervous system.