van der Heide Anouk, Dommershuijsen Lisanne J, Puhlmann Lara M C, Kalisch Raffael, Bloem Bastiaan R, Speckens Anne E M, Helmich Rick C
Radboud University Medical Centre, Department of Neurology, Centre of Expertise for Parkinson & Movement Disorders, Nijmegen, the Netherlands.
Radboud University, Donders Institute for Brain Cognition and Behavior, Centre for Cognitive Neuroimaging, Nijmegen, the Netherlands.
NPJ Parkinsons Dis. 2024 Apr 11;10(1):81. doi: 10.1038/s41531-024-00692-4.
People with Parkinson's disease (PD) are sensitive to effects of long-term stress, but might differ in stress resilience, i.e. the ability to maintain mental health despite adversity. It is unclear whether stress resilience in PD is predominantly determined by dopamine deficiency, psychosocial factors, or both. In PD animal models, chronic stressors accelerate disease progression, but evidence in humans is lacking. Our objectives were to (1) distinguish stressor-reactive from resilient PD patients, (2) identify resilience factors, and (3) compare symptom progression between stressor-reactive and resilient patients. We conducted a longitudinal survey in Personalized Parkinson Project participants (N = 350 PD). We used the COVID-19 pandemic as a model of a stressor, aligned in time for the entire cohort. COVID-19-related stressors, perceived stress, and PD symptoms were assessed at 11 timepoints (April-October 2020). Both pre-COVID and in-COVID clinical assessments were available. We quantified stressor-reactivity as the residual between actual and predicted perceived stress relative to COVID-19-related stressors, and modeled trajectories of stressor-reactivity across timepoints. We explored pre-COVID predictors of 6-month average stressor-reactivity, and tested whether stressor-reactivity was prospectively associated with one-year clinical progression rates. Latent class trajectory models distinguished patients with high (N = 123) or low (N = 227) stressor-reactivity. Pre-existing anxiety, rumination and non-motor symptom severity predicted high stressor-reactivity (risk factors), whereas quality of life, social support, positive appraisal style and cognitive abilities predicted low stressor-reactivity (resilience factors). PD-specific factors, e.g. disease duration, motor severity, and levodopa use, did not predict stressor-reactivity. The COVID-19 pandemic did not accelerate disease progression, but worsened depressive symptoms in stressor-reactive PD patients.
帕金森病（PD）患者对长期压力的影响较为敏感，但在压力恢复力方面可能存在差异，即尽管面临逆境仍能保持心理健康的能力。目前尚不清楚PD患者的压力恢复力主要是由多巴胺缺乏、心理社会因素还是两者共同决定的。在PD动物模型中，慢性应激源会加速疾病进展，但缺乏人类相关证据。我们的目标是：（1）区分应激源反应性PD患者和恢复力强的PD患者；（2）识别恢复力因素；（3）比较应激源反应性患者和恢复力强的患者之间的症状进展。我们对个性化帕金森项目参与者（N = 350例PD患者）进行了纵向调查。我们将新冠疫情作为应激源模型，对整个队列进行同步研究。在11个时间点（2020年4月至10月）评估了与新冠疫情相关的应激源、感知压力和PD症状。同时可获取疫情前和疫情期间的临床评估数据。我们将应激源反应性量化为相对于与新冠疫情相关应激源的实际感知压力与预测感知压力之间的残差，并对各时间点的应激源反应性轨迹进行建模。我们探讨了疫情前6个月平均应激源反应性的预测因素，并测试了应激源反应性是否与一年临床进展率存在前瞻性关联。潜在类别轨迹模型区分出了应激源反应性高（N = 123）或低（N = 227）的患者。既往存在的焦虑、反复思考和非运动症状严重程度可预测高应激源反应性（风险因素），而生活质量、社会支持、积极评价方式和认知能力可预测低应激源反应性（恢复力因素）。PD特异性因素，如病程、运动严重程度和左旋多巴使用情况，并不能预测应激源反应性。新冠疫情并未加速疾病进展，但应激源反应性PD患者的抑郁症状有所加重。
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