• Sandro Zambito-Marsala, Roberto Erro, Ruggero Bacchin, Annalisa Fornasier, Federico Fabris, Cecilia Lo Cascio, Franco Ferracci, Francesca Morgante, and Michele Tinazzi.
• Neurology, San Martino Hospital, Belluno, Italy.
• Parkinsonism Relat. Disord. 2017 Jan 1; 34: 43-48.

BackgroundSeveral 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.ObjectiveTo assess whether abnormalities of nociceptive inputs occur at central and/or peripheral level in pain-free PD patients with hemiparkinson using Nd:YAP LEPs.MethodsWe 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.ResultsPD 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.ConclusionsThese 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.Copyright © 2016. Published by Elsevier Ltd.

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