Yang Yifan, Cheng Yuqi, Wang Xiangyu, Upreti Bibhuti, Cui Ruomei, Liu Shuang, Shan Baoci, Yu Hongjun, Luo Chunrong, Xu Jian
Department of Rheumatology and Immunology, First Affiliated Hospital of Kunming Medical University, Kunming, China.
Department of Psychiatry, First Affiliated Hospital of Kunming Medical University, Kunming, China.
Front Neurol. 2021 Sep 16;12:662497. doi: 10.3389/fneur.2021.662497. eCollection 2021.
Hyperuricemia is the cause of gout. The antioxidant and neuroprotective effects of uric acid seem to benefit some patients with central nervous system injury. However, changes in the brain structure have not been discovered in patients with gout. Clarify the changes in cortical thickness in patients with gout and the alteration of the structural covariance networks (SCNs) based on cortical thickness. We collected structural MRIs of 23 male gout patients and 23 age-matched healthy controls. After calculating and comparing the difference in cortical thickness between the two groups, we constructed and analyzed the cortical thickness covariance networks of the two groups, and we investigated for any changes in SCNs of gout patients. Gout patients have thicker cortices in the left postcentral, left supramarginal, right medial temporal, and right medial orbitofrontal regions; and thinner cortices were found in the left insula, left superior frontal, right pericalcarine, and right precentral regions. In SCN analysis, between-group differences in global network measures showed that gout patients have a higher global efficiency. In regional network measures, more nodes in gout patients have increased centrality. In network hub analysis, we found that the transfer of the core hub area, rather than the change in number, may be the characteristic of the gout's cortical thickness covariance network. This is the first study on changes in brain cortical thickness and SCN based on graph theory in patients with gout. The present study found that, compared with healthy controls, gout patients show regional cortical thinning or thickening, and variation in the properties of the cortical thickness covariance network also changed. These alterations may be the combined effect of disease damage and physiological compensation. More research is needed to fully understand the complex underlying mechanisms of gout brain variation.
高尿酸血症是痛风的病因。尿酸的抗氧化和神经保护作用似乎对一些中枢神经系统损伤患者有益。然而，痛风患者尚未发现脑结构的变化。基于皮质厚度，阐明痛风患者皮质厚度的变化以及结构协方差网络（SCNs）的改变。我们收集了23名男性痛风患者和23名年龄匹配的健康对照者的结构磁共振成像（MRI）。在计算并比较两组之间皮质厚度的差异后，我们构建并分析了两组的皮质厚度协方差网络，并研究了痛风患者SCNs的任何变化。痛风患者在左侧中央后回、左侧缘上回、右侧颞中回和右侧眶额内侧回区域的皮质较厚；而在左侧岛叶、左侧额上回、右侧距状周围和右侧中央前回区域发现皮质较薄。在SCN分析中，组间全局网络测量的差异表明痛风患者具有更高的全局效率。在区域网络测量中，痛风患者更多的节点具有更高的中心性。在网络枢纽分析中，我们发现核心枢纽区域的转移而非数量的变化可能是痛风皮质厚度协方差网络的特征。这是第一项基于图论对痛风患者脑皮质厚度和SCNs变化的研究。本研究发现，与健康对照相比，痛风患者表现出区域皮质变薄或增厚，并且皮质厚度协方差网络属性的变化也发生了改变。这些改变可能是疾病损伤和生理补偿的综合作用。需要更多的研究来充分理解痛风脑变化的复杂潜在机制。
