Can a dysfunction of the basal ganglia and related low level nociceptive network underlie some central neuropathic pain symptoms in Parkinson’s disease?

Veronique Coizet (France), Paul Overton (UK)

Pain is a very common and troublesome, but poorly understood symptom in Parkinson’s disease (PD). Central neuropathic pain in PD is often described by patients as otherwise unexplained painful sensations with no apparent origin, predominantly on the more affected side. Central neuropathic pain is thought to originate from a dysfunction of the central nervous system suggesting that the brain circuits that allow us to perceive and process pain could be dysfunctional in Parkinson’s disease. While abnormal nociceptive processing has been reported in some cortical structures involved in pain, there is to date no clear pathophysiological mechanism to explain these specific symptoms. Based on our recent discovery of a novel nociceptive network, we propose to test a new hypothesis linking central neuropathic pain symptoms to abnormal activity of this nociceptive network between the basal ganglia, a group of structures known to be dysfunctional in Parkinson’s disease, and a primary nociceptive structure within the brainstem, the parabrachial nucleus. We also propose to test whether this network could underlie the beneficial effect of deep brain stimulation of the subthalamic nucleus on central pain symptoms.

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