Zambito-Marsala Sandro, Erro Roberto, Bacchin Ruggero, Fornasier Annalisa, Fabris Federico, Lo Cascio Cecilia, Ferracci Franco, Morgante Francesca, Tinazzi Michele
Neurology, San Martino Hospital, Belluno, Italy.
Department of Neuroscience, Biomedicine and Movement Science, University of Verona, Verona, Italy; Sobell Department of Motor Neuroscience and Movement Disorders, UCL Institute of Neurology, London, United Kingdom.
Parkinsonism Relat Disord. 2017 Jan;34:43-48. doi: 10.1016/j.parkreldis.2016.10.019. Epub 2016 Oct 24.
Several studies documented abnormal nociceptive processing in PD patients. Pain central pathways are accessible by laser-evoked potentials (LEPs). LEPs recording show a N2/P2 complex mostly generated by the anterior cingulate cortex, preceded by an earlier negative component (N1), originating from the opercular cortex. Previous work demonstrated N2/P2 amplitude reduction in PD patients and suggested a centrally-acting pathomechanism for the genesis of pain. However, since a peripheral deafferentation has been recently demonstrated in PD, it is not clear if such LEP abnormalities reflect a mechanism acting centrally or not.
To assess whether abnormalities of nociceptive inputs occur at central and/or peripheral level in pain-free PD patients with hemiparkinson using Nd:YAP LEPs.
We recorded scalp Nd:YAP-LEPs to hand stimulation in 13 pain-free patients with unilateral PD and in 13 healthy subjects. Additionally, we collected laser pain-rating in both groups.
PD patients and normal subjects showed comparable N1, N2 and P2 latencies. The N2/P2 amplitude was significantly lower in PD patients than in controls, regardless of the clinically affected side, whereas the N1/P1 amplitude was not different. PD patients had higher pain-rating, indicative of hyperalgesia.
These findings demonstrate that in the PD patients the abnormal processing of pain stimuli occurs at central rather than peripheral level. The co-existence of hyperalgesia and reduced amplitude of the N2/P2 complex, in spite of a normal N1/P1 component, suggests an imbalance between the medial and lateral pain systems. Such a dissociation might explain the genesis of central pain in PD.
多项研究记录了帕金森病（PD）患者存在异常的伤害性感受处理过程。疼痛中枢通路可通过激光诱发电位（LEP）进行检测。LEP记录显示，N2/P2复合波主要由前扣带回皮层产生，在其之前有一个更早的负向成分（N1），起源于岛盖皮层。先前的研究表明PD患者的N2/P2波幅降低，并提示疼痛发生存在中枢作用的病理机制。然而，由于最近已证实在PD患者中存在外周传入神经阻滞，目前尚不清楚这种LEP异常是否反映了中枢作用机制。
使用Nd:YAP激光诱发电位评估无痛性偏侧帕金森病患者在中枢和/或外周水平是否存在伤害性传入异常。
我们记录了13例单侧PD无痛患者和13名健康受试者手部刺激时的头皮Nd:YAP激光诱发电位。此外，我们还收集了两组的激光疼痛评分。
PD患者和正常受试者的N1、N2和P2潜伏期相当。无论临床受累侧别如何，PD患者的N2/P2波幅均显著低于对照组，而N1/P1波幅无差异。PD患者的疼痛评分更高，提示存在痛觉过敏。
这些发现表明，PD患者疼痛刺激的异常处理发生在中枢而非外周水平。尽管N1/P1成分正常，但痛觉过敏与N2/P2复合波幅降低并存，提示内侧和外侧疼痛系统之间存在失衡。这种分离现象可能解释了PD患者中枢性疼痛的发生机制。
