Roger Gilbertson Endowed Chair in Neurology, Department of Neurology, University of North Dakota School of Medicine & Health Science, and Sanford Health, Fargo, ND, United States.
Int Rev Neurobiol. 2020;153:187-211. doi: 10.1016/bs.irn.2020.03.031. Epub 2020 Jun 9.
Parkinson's disease (PD) patients exhibit strong placebo responses in clinical trials. Patient characteristics that affect placebo include patients' expectations of good outcomes, genetic variants, and personality. The presence of motor fluctuation and high baseline UPDRS motor scores predicted placebo response. However, gender, age, duration of PD, religion, or level of education do not correlate with placebo response. PD patients who are preconditioned with active treatment such as apomorphine have more robust placebo effects. Studies that focused on patients with motor fluctuations, surgical intervention, or higher probability of placebo assignment had higher rates of placebo response. Patients view participating in placebo-controlled trials positively. Placebo effect can be measured objectively using neuroimaging and neurophysiological techniques. PET studies show that placebo-induced improvement is associated with dopamine release in the dorsal striatum and that the expectation of receiving the reward, not the reward itself, increased dopamine release in the ventral striatum. Expectations of benefitting from repetitive transcranial magnetic stimulation also induced dopamine release. Expectations of receiving a dopaminergic drug induced changes in fMRI in a reward-learning task. Single cell recordings demonstrate that placebo response is associated with changes of single neuronal activities in the basal ganglia circuit. These studies demonstrate that placebo effects are genuine biological responses to the administration of placebo. In clinical trials, we can use several approaches to minimize placebo responses. In clinical practice, we can use approaches to harness the power of placebo and minimize nocebo effects to improve patients' outcome.
帕金森病（PD）患者在临床试验中表现出强烈的安慰剂反应。影响安慰剂反应的患者特征包括患者对良好结果的期望、遗传变异和个性。运动波动和高基线 UPDRS 运动评分的存在预测了安慰剂反应。然而，性别、年龄、PD 持续时间、宗教或教育水平与安慰剂反应无关。接受过诸如阿朴吗啡等活性治疗预处理的 PD 患者具有更强的安慰剂效应。专注于有运动波动、手术干预或更高安慰剂分配概率的患者的研究具有更高的安慰剂反应率。患者对参与安慰剂对照试验持积极态度。可以使用神经影像学和神经生理学技术客观地测量安慰剂效应。PET 研究表明，安慰剂诱导的改善与背侧纹状体中多巴胺的释放有关，并且对接受奖励的期望而不是奖励本身增加了腹侧纹状体中多巴胺的释放。对重复经颅磁刺激有益的期望也诱导了多巴胺的释放。对接受多巴胺能药物的期望在奖励学习任务中引起 fMRI 的变化。单细胞记录表明，安慰剂反应与基底神经节回路中单神经元活动的变化有关。这些研究表明，安慰剂效应是对安慰剂给药的真正生物学反应。在临床试验中，我们可以使用几种方法来最小化安慰剂反应。在临床实践中，我们可以利用安慰剂的力量并最小化不良反应来改善患者的预后。
