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Pain sensitivity in Parkinson's disease is known to be altered in an L-dopa-dependent manner with increased spinal nociception and experimental pain perception in the medication-defined "off" state. As Parkinson's disease-related pain can be an early symptom in Parkinson's disease, the present study aimed to investigate experimental pain sensitivity and spinal nociception during clinical progression. The nociceptive flexion reflex as a marker of spinal nociception as well as electrical and heat pain thresholds were assessed during the medication-defined "off" state in 29 patients with Parkinson's disease divided into 3 severity groups (according to their Unified Parkinson's Disease Rating Scale motor score) and compared with 27 healthy elderly subjects. Parkinson's disease-related pain was also quantified. Data provided evidence that spinal nociception and pain sensitivity are preserved during the early phase of Parkinson's disease. Following increased spinal nociception (F(1,36) = 6.838, P = .013), experimental thermal and electrical pain sensitivity were augmented during the course of Parkinson's disease (F(1,34) = 5.397, P = .014; F(1,34) = 6.038, P = 0.053), whereas spinal nociception further increased (F(1,34) = 5.397, P < .001). Increased experimental pain sensitivity was observed in patients exhibiting Parkinson's disease-related pain. Spinal alterations either on the local level or induced by diminished dopaminergic descending inhibition probably led to increased pain sensitivity in later stages. Because Parkinson's disease-related pain is correlated with experimental pain sensitivity these 2 observations likely reflect a causal relation.