The present research investigates factors contributing to bradykinesia in the control of simple and complex voluntary limb movement in Parkinson's disease (PD) patients. The functional scheme of the basal ganglia (BG)-thalamocortical circuit was described by a mathematical model based on the mean firing rates of BG nuclei. PD was simulated as a reduction in dopamine levels, and a loss of functional segregation between two competing motor modules. In order to compare model simulations with performed movements, flexion and extension at the elbow joint is taken as a test case. Results indicated that loss of segregation contributed to bradykinesia due to interference between competing modules and a reduced ability to suppress unwanted movements. Additionally, excessive neurotransmitter depletion is predicted as a possible mechanism for the increased difficulty in performing complex movements. The simulation results showed that the model is in qualitative agreement with the results from movement experiments on PD patients and healthy subjects. Furthermore, based on changes in the firing rate of BG nuclei, the model demonstrated that the effective mechanism of Deep Brain Stimulation (DBS) in STN may result from stimulation induced inhibition of STN, partial synaptic failure of efferent projections, or excitation of inhibitory afferent axons even though the underlying methods of action may be quite different for the different mechanisms.

中文翻译：

---

帕金森病患者运动迟缓增加，运动复杂性增加：肘部屈伸运动。

本研究调查了在控制帕金森病 (PD) 患者简单和复杂的随意肢体运动中导致运动迟缓的因素。基底神经节 (BG)-丘脑皮质回路的功能方案由基于 BG 核的平均放电率的数学模型描述。PD 被模拟为多巴胺水平的降低，以及两个相互竞争的运动模块之间功能隔离的丧失。为了将模型模拟与执行的运动进行比较，将肘关节的屈伸作为测试案例。结果表明，由于竞争模块之间的干扰和抑制不需要的运动的能力降低，隔离的丧失导致了运动迟缓。此外，神经递质过度消耗被预测为执行复杂运动难度增加的可能机制。仿真结果表明，该模型与 PD 患者和健康受试者的运动实验结果定性一致。此外，基于 BG 核放电率的变化，该模型证明 STN 中深部脑刺激 (DBS) 的有效机制可能是刺激诱导的 STN 抑制、传出投射的部分突触失败或抑制性传入的兴奋。尽管对于不同的机制，轴突的基本作用方法可能大不相同。仿真结果表明，该模型与 PD 患者和健康受试者的运动实验结果定性一致。此外，基于 BG 核放电率的变化，该模型证明 STN 中深部脑刺激 (DBS) 的有效机制可能是刺激诱导的 STN 抑制、传出投射的部分突触失败或抑制性传入的兴奋。尽管对于不同的机制，轴突的基本作用方法可能大不相同。仿真结果表明，该模型与 PD 患者和健康受试者的运动实验结果定性一致。此外，基于 BG 核放电率的变化，该模型证明 STN 中深部脑刺激 (DBS) 的有效机制可能是刺激诱导的 STN 抑制、传出投射的部分突触失败或抑制性传入的兴奋。尽管对于不同的机制，轴突的基本作用方法可能大不相同。