Mole Jilu Princy, Subramanian Leena, Bracht Tobias, Morris Huw, Metzler-Baddeley Claudia, Linden David E J
Cardiff University Brain Research Imaging Centre (CUBRIC), School of Psychology, Cardiff University, Cardiff, UK.
Institute of Psychological Medicine and Clinical Neurosciences (IPMCN), School of Medicine, Cardiff University, Cardiff, UK.
Eur Radiol. 2016 Oct;26(10):3327-35. doi: 10.1007/s00330-015-4178-1. Epub 2016 Jan 15.
To determine the differences in motor pathways and selected non-motor pathways of the basal ganglia in Parkinson's disease (PD) patients compared to healthy controls (HCs).
We analysed diffusion weighted imaging data of 24 PD patients and 26 HCs. We performed deterministic tractography analysis using the spherical deconvolution-based damped Richardson-Lucy algorithm and subcortical volume analysis.
We found significantly increased fractional anisotropy (FA) in the motor pathways of PD patients: the bilateral corticospinal tract (right; corrected p = 0.0003, left; corrected p = 0.03), bilateral thalamus-motor cortex tract (right; corrected p = 0.02, left; corrected p = 0.004) and the right supplementary area-putamen tract (corrected p = 0.001). We also found significantly decreased FA in the right uncinate fasiculus (corrected p = 0.01) and no differences of FA in the bilateral supero-lateral medial forebrain bundles (p > 0.05) of PD patients compared to HCs. There were no subcortical volume differences (p > 0.05) between the PD patients and HCs.
These results can inform biological models of neurodegeneration and neuroplasticity in PD. We suggest that increased FA values in the motor tracts in PD may reflect compensatory reorganization of neural circuits indicative of adaptive or extended neuroplasticity.
• Fractional anisotropy was higher in motor pathways of PD patients compared to healthy controls. • Fractional anisotropy was lower in the uncinate fasciculus of PD patients compared to healthy controls. • Increased fractional anisotropy could suggest adaptive neuroplasticity or selective neurodegeneration.
确定帕金森病(PD)患者与健康对照者(HCs)相比,基底神经节运动通路和选定的非运动通路的差异。
我们分析了24例PD患者和26例HCs的扩散加权成像数据。我们使用基于球面反卷积的阻尼理查森-露西算法进行确定性纤维束成像分析和皮质下体积分析。
我们发现PD患者运动通路中的分数各向异性(FA)显著增加:双侧皮质脊髓束(右侧;校正p = 0.0003,左侧;校正p = 0.03)、双侧丘脑-运动皮质束(右侧;校正p = 0.02,左侧;校正p = 0.004)以及右侧辅助运动区-壳核束(校正p = 0.001)。我们还发现PD患者右侧钩束的FA显著降低(校正p = 0.01),与HCs相比,PD患者双侧上外侧内侧前脑束的FA无差异(p > 0.05)。PD患者和HCs之间没有皮质下体积差异(p > 0.05)。
这些结果可为PD神经退行性变和神经可塑性的生物学模型提供信息。我们认为PD患者运动束中FA值的增加可能反映了神经回路的代偿性重组,这表明存在适应性或扩展性神经可塑性。
• 与健康对照者相比,PD患者运动通路中的分数各向异性更高。• 与健康对照者相比,PD患者钩束中的分数各向异性更低。• 分数各向异性增加可能提示适应性神经可塑性或选择性神经退行性变。