Electrophysiological Evidence for Impaired Central Pain Modulation in Parkinson's Disease

Background There is a remarkable overlap between structures involved in pain perception and the pathophysiology of Parkinson's disease (PD). Recent efforts to allocate pain into mechanistic subtypes require a better understanding of central pain processing in PD patients. Objectives The aim of this study was to show electrophysiological evidence for altered central pain processing in a patient group with PD, taking their reported pain, somatosensory profile, and motor symptoms as well as pharmacotherapy into account. Methods The laser‐evoked‐potential (LEP)‐habituation paradigm and quantitative sensory testing were applied to PD patients (n = 41) in the off‐ l ‐dopamine (levodopa) state. The development of LEP amplitudes and laser pain ratings over the course of 100 painful stimuli was compared to those of an age‐matched control group (n = 24). The Unified Parkinson's Disease Rating Scale (UPDRS) III and the painDETECT questionnaire and medical history, including pharmacotherapy, were assessed and analyzed in context with LEP and pain habituation aiming to find an electrophysiological proxy for central sensitization. Results Patients exhibited a significantly reduced capacity for LEP habituation regardless of clinically reported pain and sensory profile. No association of EEG data has been found with the mean l ‐DOPA equivalent dose taken by the patients. Conclusions We hereby report electrophysiological evidence for an impaired central pain modulation in PD patients regardless of pain presentation and individual sensation. Further exploration of abnormal central pain processing in PD using methods like the LEP habituation paradigm or conditioned pain modulation protocol is needed in larger cohorts.