Bradykinesia, or slowness of movement, is a defining feature of Parkinson disease (PD) and a major contributor to the negative effects on quality of life associated with this disorder and related conditions. A dominant pathophysiological model of bradykinesia in PD has existed for approximately 30 years and has been the basis for the development of several therapeutic interventions, but accumulating evidence has made this model increasingly untenable. Although more recent models have been proposed, they also appear to be flawed. In this Perspective, I consider the leading prior models of bradykinesia in PD and argue that a more functionally related model is required, one that considers changes that disrupt the fundamental process of accurate information transmission. In doing so, I review emerging evidence of network level functional connectivity changes, information transfer dysfunction and potential motor code transmission error and present a novel model of bradykinesia in PD that incorporates this evidence. I hope that this model may reconcile inconsistencies in its predecessors and encourage further development of therapeutic interventions.

运动迟缓或运动缓慢是帕金森病 (PD) 的一个定义特征，也是对与这种疾病和相关病症相关的生活质量产生负面影响的主要原因。 PD 运动迟缓的主要病理生理学模型已存在约 30 年，并且是多种治疗干预措施开发的基础，但越来越多的证据使该模型越来越站不住脚。尽管已经提出了更新的模型，但它们似乎也存在缺陷。在本视角中，我考虑了 PD 运动迟缓的主要先前模型，并认为需要一种功能更相关的模型，该模型考虑破坏准确信息传输基本过程的变化。在此过程中，我回顾了网络级功能连接变化、信息传输功能障碍和潜在的运动代码传输错误的新证据，并提出了一种包含这些证据的帕金森病运动迟缓的新模型。我希望这个模型可以解决其前身的不一致之处，并鼓励治疗干预措施的进一步发展。