Altered nociceptive processing in the context of Parkinson's disease

Pain is highly prevalent in Parkinson’s disease and includes central neuropathic pain described by Parkinson’s disease patients as bizarre and unexplained painful sensations predominating on the more affected side. The presence of central neuropathic pain in Parkinson’s disease suggests that the brain circuits that allow us to process pain could be dysfunctional in the disorder. However, there is to date no clear pathophysiological mechanism to explain these symptoms. I suggested these central neuropathic pain could be due to a dysfunction of the link between the basal ganglia and primary nociceptive structures from the brainstem. I will present evidences that the dysfunction of the subthalamic nucleus and/or substantia nigra pars reticulata, two major structures of the basal ganglia, may impact nociceptive processing in the parabrachial nucleus, a low level primary nociceptive structure in the brainstem, and induce a cellular and molecular neuro-adaptation in this structure. I will then explain the significance of these results in the development of central neuropathic pain in Parkinson’s disease.