Objective: To investigate whether central pain processing is altered in “drug-naive” pain-free Parkinson disease (dnPD) patients.

Background: Despite its clinical relevance, the pathophysiology of pain in PD is still largely unknown, and both central and peripheral mechanisms have been invoked. Previous behavioural and neurophysiological studies have reported a reduced pain threshold in PD patients with or without pain symptoms.

Methods: Using event-related fMRI, functional response to forearm heat stimulation (FHS) at two different intensities (41° and 53 °C) was investigated in 20 pain-free dnPD patients, compared with pain-free healthy controls (HCs). After each fMRI session each subject was asked to rate verbally the intensity of pain induced by the experimental stimulus by means of a numerical rating scale (NRS) ranging from 0 (‘‘no pain’’) to 10 (‘‘worst pain imaginable’’). Voxel-based morphometry was used to explore potential structural differences. Secondary analyses evaluated associations between BOLD signal changes and PD clinical features and behavioural responses.

Results: During low-innocuous FHS (41°C), no activation differences were shown between dnPD patients and HCs. Instead, during high-noxious FHS (53°C) a significantly increased activation in the left somatosensory cortex, left cerebellum (lingula) and right low pons was observed in dnPD patients when compared to HCs. Interestingly, no statistically significant difference in experimental pain perception was detected between dnPD patients and HCs. However, during high-noxious FHS, a significant negative correlation was found between BOLD signal change in the right low pons (p<0.05; r=-0.8) and NRS scores of experimental pain stimulus only in dnPD patients. No structural abnormalities were detected between the two experimental groups.

Conclusions: Our findings suggest that a functional remodulation of pain processing pathways occurs even in the absence of clinically overt pain symptoms in dnPD patients. These functional changes may represent an additional recruitment of descending pain modulatory systems to meet analgesic demands and to maintain proficiency in an early stage of the disease. We hypothesize that this compensatory reorganization may eventually become dysfunctional over time, contributing to the emergence of pain symptoms in more advanced disease stages.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/central-pain-processing-in-drug-naive-pain-free-patients-with-parkinsons-disease/