Abnormal nociceptive processing occurs centrally and not peripherally in pain-free Parkinson disease patients: A study with laser-evoked potentials.
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.
Neurology, San Martino Hospital, Belluno, Italy.
Sandro
S
Zambito-Marsala
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.
Roberto
R
Erro
Department of Neuroscience, Biomedicine and Movement Science, University of Verona, Verona, Italy.
Ruggero
R
Bacchin
Neurology, San Martino Hospital, Belluno, Italy.
Annalisa
A
Fornasier
Neurology, San Martino Hospital, Belluno, Italy.
Federico
F
Fabris
Neurology, San Martino Hospital, Belluno, Italy.
Cecilia
C
Lo Cascio
Neurology, San Martino Hospital, Belluno, Italy.
Franco
F
Ferracci
Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Francesca
F
Morgante
Department of Neuroscience, Biomedicine and Movement Science, University of Verona, Verona, Italy. Electronic address: michele.tinazzi@univr.it.
Michele
M
Tinazzi
D000368:Aged; D000704:Analysis of Variance; D004569:Electroencephalography; D005260:Female; D007839:Functional Laterality; D006801:Humans; D066331:Laser-Evoked Potentials / Q000502:physiology*; D007834:Lasers / Q000009:adverse effects; D008297:Male; D008875:Middle Aged; D059225:Nociception / Q000502:physiology*; D010146:Pain / Q000503:physiopathology; D017288:Pain Threshold / Q000502:physiology*; D010300:Parkinson Disease / Q000503:physiopathology*; D011601:Psychophysics; D011930:Reaction Time / Q000502:physiology
Hyperalgesia; Laser evoked potentials; Nd:YAP; Nociception; Pain; Parkinson disease; Somatosensory system