Impaired pain processing in Parkinson's disease and its relative association with the non-motor symptom

背景和目的：许多非运动症状与帕金森病(PD)有关。其中，疼痛和嗅觉障碍往往是常见的运动前症状。帕金森病已被证明表现出异常的中枢疼痛处理，尽管其潜在的机制尚未完全了解。为了进一步研究这一点，我们用皮内针电极对帕金森病患者进行了特异性A-δ刺激并测定了其嗅觉功能。方法：对42例帕金森病患者(男18例，女24例)和11例健康对照组(男8例，女3例)进行了研究。用细针电极刺激表皮A-δ纤维，并在顶端记录体感诱发电位。结果：尽管N1/P1峰间波幅明显降低(p&lt；0)，但N1潜伏期和P1潜伏期无显著差异(P>0.05)。帕金森病患者与正常对照组比较差异无统计学意义。在PD患者中，N1/P1波幅与病程显著相关(r=-0。35，p&lt；0。05)，Hoehn-Yahr阶段(r=-0。38，p&lt；0。05)和UPDRS第III部分(r=-0.42，p&lt；0。01)。此外，OSIT-J评分与SEP波幅相关(r=0。41，p&lt；0。结论：特异性伤害性刺激A-δ纤维可损害帕金森病患者的痛觉加工，并与嗅觉功能障碍密切相关。我们认为这一机制可能涉及PD病理过程中的边缘系统。

Background and purpose : Many non-motor symptoms are associated with Parkinson's disease(PD). Of these, pain and olfactory disturbance tend to be common premotor symptoms. PD has been shown to exhibit abnormal central pain processing, although underlying mechanisms are not yet fully understood. In order to investigate this further, we assessed PD patients by specific Aδstimulation with intra-epidermal needle electrode and determined olfactory function.Methods : Forty-two patients(18 males and 24 females) with PD and 11 healthy control subjects(8 males and 3 females) were studied. A thin needle electrode was used to stimulate epidermal Aδfibers, and somatosensory evoked potentials(SEPs) recorded at the vertex. Olfactory function was evaluated using the Odor Stick Identification Test for Japanese(OSIT-J) and its relationship with pain-related SEPs was investigated.Results : There were no significant differences in N1 latencies or P1 latencies although N1/P1 peak-to-peak amplitudes were significantly lower(p<0. 05) in PD patients than in control subjects. In PD patients, there were significant correlations between N1/P1 amplitudes and disease duration(r=-0. 35, p<0. 05), Hoehn-Yahr stage(r=-0. 38, p<0. 05) and UPDRS part III(r=-0. 42, p<0. 01). Furthermore, the OSIT-J scores correlated with SEP amplitude(r=0. 41, p<0. 01).Conclusion : Pain processing in PD patients was impaired under specific nociceptive stimulation of Aδfibers and significant correlation with smell dysfunction was detected. We suggest that this mechanism may involve the limbic system during PD pathology.