Sandro Zambito-Marsala1, Roberto Erro2, Ruggero Bacchin3, Annalisa Fornasier1, Federico Fabris1, Cecilia Lo Cascio1, Franco Ferracci1, Francesca Morgante4, Michele Tinazzi5. 1. Neurology, San Martino Hospital, Belluno, Italy. 2. 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. 3. Department of Neuroscience, Biomedicine and Movement Science, University of Verona, Verona, Italy. 4. Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy. 5. Department of Neuroscience, Biomedicine and Movement Science, University of Verona, Verona, Italy. Electronic address: michele.tinazzi@univr.it.
Abstract
BACKGROUND: 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. OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: Several studies documented abnormal nociceptive processing in PDpatients. 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 PDpatients 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. OBJECTIVE: To assess whether abnormalities of nociceptive inputs occur at central and/or peripheral level in pain-free PDpatients with hemiparkinson using Nd:YAP LEPs. METHODS: We recorded scalp Nd:YAP-LEPs to hand stimulation in 13 pain-freepatients with unilateral PD and in 13 healthy subjects. Additionally, we collected laser pain-rating in both groups. RESULTS:PDpatients and normal subjects showed comparable N1, N2 and P2 latencies. The N2/P2 amplitude was significantly lower in PDpatients than in controls, regardless of the clinically affected side, whereas the N1/P1 amplitude was not different. PDpatients had higher pain-rating, indicative of hyperalgesia. CONCLUSIONS: These findings demonstrate that in the PDpatients 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.
Authors: Giulia Liberati; Maxime Algoet; Anne Klöcker; Susana Ferrao Santos; Jose Geraldo Ribeiro-Vaz; Christian Raftopoulos; André Mouraux Journal: Sci Rep Date: 2018-05-29 Impact factor: 4.379