Parkinson’s disease (PD) is a progressive neurodegenerative disorder mainly characterized by bradykinesia and akinesia. Interestingly, these motor disabilities can depend on the patient emotional state. Disabled PD patients remain able to produce normal motor responses in the context of urgent or externally driven situations or even when exposed to appetitive cues such as music. To describe this phenomenon Souques coined the term “paradoxical kinesia” a century ago. Since then, the mechanisms underlying paradoxical kinesia are still unknown due to a paucity of valid animal models that replicate this phenomenon. To overcome this limitation, we established two animal models of paradoxical kinesia. Using these models, we investigated the neural mechanisms of paradoxical kinesia, with the results pointing to the inferior colliculus (IC) as a key structure. Intracollicular electrical deep brain stimulation, glutamatergic and GABAergic mechanisms may be involved in the elaboration of paradoxical kinesia. Since paradoxical kinesia might work by activation of some alternative pathway bypassing basal ganglia, we suggest the IC as a candidate to be part of this pathway.

中文翻译：

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悖论性运动可能不再是一个等待100年才能揭开的悖论

帕金森病（PD）是一种进行性神经退行性疾病，主要特征为运动迟缓和运动不能。有趣的是，这些运动障碍可能取决于患者的情绪状态。残疾帕金森病患者在紧急或外部驱动的情况下，甚至在暴露于音乐等食欲暗示时，仍然能够产生正常的运动反应。为了描述这种现象，苏克斯在一个世纪前创造了“矛盾运动”一词。从那时起，由于缺乏复制这种现象的有效动物模型，矛盾运动的潜在机制仍然未知。为了克服这一限制，我们建立了两种矛盾运动动物模型。使用这些模型，我们研究了矛盾运动的神经机制，结果表明下丘（IC）是一个关键结构。丘内深部脑电刺激、谷氨酸能和 GABA 能机制可能参与了矛盾运动的形成。由于矛盾运动可能通过激活一些绕过基底神经节的替代途径来发挥作用，因此我们建议 IC 作为该途径的一部分的候选者。