Radiological Sciences, Division of Clinical Neuroscience, University of Nottingham, Nottingham, NG7 2UH, UK.
Sir Peter Mansfield Imaging Centre, University of Nottingham, Nottingham, NG7 2UH, UK.
Brain Imaging Behav. 2020 Aug;14(4):1263-1280. doi: 10.1007/s11682-019-00061-3.
To investigate factors affecting the pattern of motor brain activation reported in people with Parkinson's (PwP), aiming to differentiate disease-specific features from treatment effects.
A co-ordinate-based-meta-analysis (CBMA) of functional motor neuroimaging studies involving patients with Parkinson's (PwP), and healthy controls (HC) identified 126 suitable articles. The experiments were grouped based on subject feature, medication status (onMed/offMed), deep brain stimulation (DBS) status (DBSon/DBSoff) and type of motor initiation.
HC and PwP shared similar neural networks during upper extremity motor tasks but with differences of reported frequency in mainly bilateral putamen, insula and ipsilateral inferior parietal and precentral gyri. The activation height was significantly reduced in the bilateral putamen, left SMA, left subthalamus nucleus, right thalamus and right midial global pallidum in PwP (vs. HC), and pre-SMA hypoactivation correlated with disease severity. These changes were not found in patients on dopamine replacement therapy (PwP vs. HC) in line with a restorative function. By contrast, left SMA and primary motor cortex showed hyperactivation in the medicated state (vs. HC) suggesting dopaminergic overcompensation. Deep-brain stimulation (PwP during the high frequency subthalamus nucleus (STN) DBS vs. no stimulation) induced a decrease in left SMA activity and the expected increase in the left subthalamic/thalamic region regardless of hand movement. We further demonstrated a disease related effect of motor intention with only PwP showing increased activation in the medial frontal lobe in self-initiated studies.
We describe a consistent disease-specific pattern of putaminal hypoactivation during motor tasks that appears reversed by dopamine replacement. Inconsistent reports of altered SMA/pre-SMA activation can be explained by task- and medication-specific variation in intention. Moreover, SMA activity was reduced during STN-DBS, while dopamine-induced hyperactivation of SMA which might underpin hyperdynamic L-dopa related overcompensation.
探究影响帕金森病（PwP）患者大脑运动区激活模式的因素，旨在区分疾病特异性特征与治疗效果。
对涉及帕金森病患者（PwP）和健康对照（HC）的功能性运动神经影像学研究进行基于坐标的荟萃分析（CBMA），共确定了 126 篇合适的文章。根据受试者特征、用药状态（用药/停药）、深部脑刺激（DBS）状态（DBSon/DBSoff）和运动起始类型对实验进行分组。
HC 和 PwP 在进行上肢运动任务时共享相似的神经网络，但在双侧壳核、岛叶和同侧顶下小叶和中央前回的报告频率存在差异。与 HC 相比，PwP 的双侧壳核、左侧 SMA、左侧丘脑底核、右侧丘脑和右侧内侧苍白球激活高度显著降低，且前扣带皮层的低激活与疾病严重程度相关。在接受多巴胺替代治疗的患者中（PwP 与 HC 相比）未发现这些变化，这与恢复功能相符。相反，在用药状态下，左侧 SMA 和初级运动皮层表现出过度激活（与 HC 相比），提示多巴胺能过度补偿。深部脑刺激（PwP 在高频丘脑底核（STN）DBS 时与无刺激时相比）导致左侧 SMA 活性降低和左丘脑底核/丘脑区域预期增加，而与手部运动无关。我们进一步证明了运动意图的疾病相关性，只有 PwP 在自主运动研究中表现出内侧额叶的激活增加。
我们描述了一种一致的与疾病相关的壳核激活减少模式，这种模式在接受多巴胺替代治疗时似乎会逆转。不一致的 SMA/pre-SMA 激活报告可以通过任务和药物特异性的意图变化来解释。此外，在 STN-DBS 期间 SMA 活性降低，而多巴胺诱导的 SMA 过度激活可能是导致 L-多巴相关过度补偿的超动态机制。
