Pain processing in Parkinson’s disease: motivational-emotional vs. sensory-discriminative components

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Pain has been reported in 30%-85% of patients with Parkinson’s disease (PD). Pain has even been described as an early symptom of PD, preceding motor symptoms by a couple of years. Standard dopaminergic medication can improve musculoskeletal pain due to rigidity and motor fluctuation, but only a third of all PD patients reports a positive effect of this medication on their pain . In line with this observation, anti-Parkinsonian medication appears not to affect pain thresholds . Although altered pain perception has been described in PD, the mechanisms underlying pain in PD remain unclear. Our hypothesis is that pain in PD is caused by impairments in the so-called medial pain system, in line with known neuroanatomical impairments in PD, resulting in alterations of motivational-emotional components of pain processing as opposed to sensory-discriminative pain components.Previous studies on pain in PD have predominantly focused on characterizing sensory-discriminative pain components and therefore responses of the lateral pain system, largely ignoring motivational-emotional pain responses. The focus on sensory-discriminative pain components in PD patients has likely been caused, at least partially, by a lack of standard paradigms focusing on emotional-motivational pain processing and not distinguishing it from sensory-discriminative pain processing. Such a paradigm has been developed and validated by Dr. Becker. In the proposed project, pain perception of PD patients during OFF and ON phases of their dopaminergic medication and of age- and sex-matched healthy controls will be assessed using this paradigm. A particular focus will be on analyzing the different components of pain processing and their alteration due to PD. To complement these assessments, brain responses related to pain processing will be studied with magnetoencephalography (MEG). We expect gamma oscillations within the medial pre-frontal cortex to encode the emotional processing of painful stimuli, while alpha and gamma oscillations within the sensorimotor regions encode the actual pain intensity. The MEG findings should provide an understanding of the mechanisms of different pain components and their modulation by dopamine in the central mechanisms of pain processing in these patients and healthy controls. The results of this project should help (1) reconcile inconsistent findings on pain in PD patients and (2) characterizing brain mechanisms of different pain components in PD. With this knowledge, it will be possible to optimize pharmacological pain treatment in Parkinson’s disease and to develop non-invasive neurofeedback approaches to reduce increased pain perception in these patients.