Joza Stephen, Camicioli Richard, Martin W R Wayne, Wieler Marguerite, Gee Myrlene, Ba Fang
Division of Neurology, Department of Medicine, University of Alberta, Edmonton, AB, Canada.
Department of Medicine, University of Alberta, Edmonton, AB, Canada.
Front Aging Neurosci. 2022 Jul 8;14:874692. doi: 10.3389/fnagi.2022.874692. eCollection 2022.
Gait impairment is a debilitating and progressive feature of Parkinson's disease (PD). Increasing evidence suggests that gait control is partly mediated by cholinergic signaling from the pedunculopontine nucleus (PPN).
We investigated whether PPN structural connectivity correlated with quantitative gait measures in PD.
Twenty PD patients and 15 controls underwent diffusion tensor imaging to quantify structural connectivity of the PPN. Whole brain analysis using tract-based spatial statistics and probabilistic tractography were performed using the PPN as a seed region of interest for cortical and subcortical target structures. Gait metrics were recorded in subjects' medication ON and OFF states, and were used to determine if specific features of gait dysfunction in PD were related to PPN structural connectivity.
Tract-based spatial statistics revealed reduced structural connectivity involving the corpus callosum and right superior corona radiata, but did not correlate with gait measures. Abnormalities in PPN structural connectivity in PD were lateralized to the right hemisphere, with pathways involving the right caudate nucleus, amygdala, pre-supplementary motor area, and primary somatosensory cortex. Altered connectivity of the right PPN-caudate nucleus was associated with worsened cadence, stride time, and velocity while in the ON state; altered connectivity of the right PPN-amygdala was associated with reduced stride length in the OFF state.
Our exploratory analysis detects a potential correlation between gait dysfunction in PD and a characteristic pattern of connectivity deficits in the PPN network involving the right caudate nucleus and amygdala, which may be investigated in future larger studies.
步态障碍是帕金森病（PD）的一种致残性且进行性的特征。越来越多的证据表明，步态控制部分由脚桥核（PPN）的胆碱能信号介导。
我们研究了PD患者中PPN的结构连接性是否与定量步态指标相关。
20例PD患者和15名对照者接受了扩散张量成像，以量化PPN的结构连接性。使用基于体素的空间统计学和概率性纤维束成像进行全脑分析，将PPN作为皮质和皮质下目标结构的感兴趣种子区域。在受试者服药“开”和“关”状态下记录步态指标，并用于确定PD中步态功能障碍的特定特征是否与PPN结构连接性相关。
基于体素的空间统计学显示，涉及胼胝体和右侧放射冠上部的结构连接性降低，但与步态指标无关。PD患者PPN结构连接性异常定位于右侧半球，涉及右侧尾状核、杏仁核、辅助运动前区和初级体感皮层的通路。右侧PPN-尾状核连接性改变与服药“开”状态下的步频、步幅时间和速度恶化有关；右侧PPN-杏仁核连接性改变与服药“关”状态下的步幅缩短有关。
我们的探索性分析检测到PD中的步态功能障碍与PPN网络中涉及右侧尾状核和杏仁核的连接缺陷特征模式之间存在潜在相关性，这可能在未来更大规模的研究中进行探究。
