White matter alterations in Parkinson's disease with levodopa-induced dyskinesia
White matter alterations in Parkinson's disease with levodopa-induced dyskinesia
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DOI：
10.1016/j.parkreldis.2021.07.021
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发表时间：
2021-07-27
影响因子：
4.1
通讯作者：
Hattori, Nobutaka
中科院分区：
文献类型：
--
作者：
Ogawa, Takashi;Hatano, Taku;Hattori, Nobutaka
前言：左旋多巴诱导的运动障碍是左旋多巴治疗的并发症，对患者的生活质量产生负面影响。我们旨在利用先进的扩散磁共振成像技术阐明左旋多巴诱导的帕金森病运动障碍的白质改变。方法：纳入临床确诊无左旋多巴致运动障碍的帕金森病患者26例，伴有左旋多巴致运动障碍的帕金森病患者25例，健康对照23例。使用3-T磁共振扫描仪对受试者进行成像。弥散张量成像、弥散峰度成像、神经突定向弥散和密度成像结果通过全脑分组方法和每个白质束的兴趣区域分析在组间进行比较。此外，使用逻辑回归分析计算左旋多巴引起的运动障碍的优势比。结果：组间基于束的空间统计分析显示，在健康对照者和无左旋多巴诱导运动障碍的帕金森病患者之间，以及有和没有左旋多巴诱导运动障碍的帕金森病患者之间，白质在各向同性扩散、复杂性或异质性以及神经突密度方面存在显著差异。使用全脑分组方法进行感兴趣区域分析显示，外囊、额枕下束、下纵束和钩状束也有类似的改变。这些束存在左旋多巴诱导的运动障碍的比值比约为2.3。结论：我们的研究结果表明，与没有左旋多巴诱导的运动障碍的帕金森病相比，伴有左旋多巴诱导的运动障碍的帕金森病产生更少的白质微结构破坏，特别是在颞叶纤维中。这些纤维对于左旋多巴诱导的运动障碍的存在具有2倍以上的优势比，并且可能与后遗症的发病机制有关。
Introduction: Levodopa-induced dyskinesia is a complication of levodopa therapy and negatively impacts the quality of life of patients. We aimed to elucidate white matter alterations in Parkinson's disease with levodopa-induced dyskinesia using advanced diffusion magnetic resonance imaging techniques. Methods: The enrolled subjects included 26 clinically confirmed Parkinson's disease patients without levodopa-induced dyskinesia, 25 Parkinson's disease patients with levodopa-induced dyskinesia, and 23 healthy controls. Subjects were imaged using a 3-T magnetic resonance scanner. Diffusion tensor imaging, diffusion kurtosis imaging, and neurite orientation dispersion and density imaging findings were compared between groups with a group-wise whole brain approach and a region-of-interest analysis for each white matter tract. Additionally, logistic regression analysis was used to calculate odds ratios for levodopa-induced dyskinesia. Results: Group-wise tract-based spatial statistical analysis revealed significant white matter differences in isotropic diffusion, complexity, or heterogeneity, and neurite density between healthy controls and Parkinson's disease patients without levodopa-induced dyskinesia and between patients with and without levodopa-induced dyskinesia. Region-of-interest analysis revealed similar alterations using a group-wise whole-brain approach in the external capsule, inferior fronto-occipital fasciculus, inferior longitudinal fasciculus, and uncinate fasciculus. These tracts had an odds ratio of approximately 2.3 for the presence of levodopa-induced dyskinesia. Conclusions: Our findings suggest that Parkinson's disease with levodopa-induced dyskinesia produces less white matter microstructural disruption, especially in temporal lobe fibers, than Parkinson's disease without levodopa-induced dyskinesia. These fibers has a more than 2-fold odds ratio for the presence of levodopa-induced dyskinesia and might be associated with the pathogenesis of the sequela.