Compensation is described as normal or near to normal performance in Parkinson's disease (PD), despite the ongoing neural loss. Functional compensation typically proceeds in an inverse U-shaped manner: compensation initiates in the prodromal phase, followed by an increasing episode until plateauing and diminishes in the advanced stages of the disease. The first evidence of the structural compensation was reported by functional magnetic resonance imaging studies. Recent studies, which have used diffusion tensor imaging (DTI) as the basis for their investigation, have shown improved white matter diffusional properties both in motor- and non-motor-related structures in association with improved clinical scores in patients with PD. The majority of DTI studies have demonstrated microstructural compensation in the prodromal/early stages of PD at the regional scale. However, there have been reports of compensation in later stages of the disease and the whole-brain/network scale that are probably due to the heterogeneous nature of PD. Although serving as a promising beginning to characterize compensation, lots remain to be clarified in understanding the underlying mechanisms of compensation and its structural pattern in PD. The existing knowledge gap necessitates studies that their main research questions are focused on structural compensation. This requirement becomes more apparent because structural compensation evidence has mostly emerged from the post hoc analysis of data and incidental findings of studies. Thus, future studies are required to investigate compensatory microstructural changes in PD to clarify the exact underlying mechanisms. These studies would also provide a basis to develop clinical improvements in the early diagnosis and management of PD.

中文翻译：

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作为帕金森病代偿机制的结构性白质改变：弥散张量成像研究的系统评价。

代偿被描述为在帕金森病 (PD) 中的正常或接近正常的表现，尽管存在持续的神经丧失。功能代偿通常以倒 U 形方式进行：代偿在前驱期开始，然后是增加的发作直至达到平台期，并在疾病的晚期阶段减弱。功能性磁共振成像研究报告了结构补偿的第一个证据。最近使用弥散张量成像 (DTI) 作为研究基础的研究表明，运动和非运动相关结构中白质扩散特性的改善与 PD 患者临床评分的改善有关。大多数 DTI 研究已经证明了区域范围内 PD 前驱/早期阶段的微观结构补偿。然而，有报道称在疾病晚期和全脑/网络尺度上有补偿，这可能是由于 PD 的异质性。尽管作为表征补偿的一个有希望的开始，但在理解补偿的潜在机制及其在 PD 中的结构模式方面仍有许多问题需要澄清。现有的知识差距需要研究他们的主要研究问题集中在结构补偿上。这一要求变得更加明显，因为结构补偿证据主要来自对数据的事后分析和研究的偶然发现。因此，未来的研究需要调查 PD 的代偿性微观结构变化，以阐明确切的潜在机制。这些研究还将为开发 PD 早期诊断和管理的临床改进提供基础。