In this study, STN-DBS raised pain thresholds and restored a better functioning of the lateral discriminative pain system in PD patients with PD-related neuropathic pain.
Painful sensations are common in Parkinson’s disease. In many patients, such sensations correspond to neuropathic pain and could be related to central alterations of pain processing. Subthalamic nuclei deep brain stimulation improves motor function in Parkinson’s disease. Several structures of the basal ganglia are involved in nociceptive function, and deep brain stimulation could thus also modify pain perception in Parkinson’s disease. To test this hypothesis, we compared subjective heat pain thresholds, in deep brain stimulation OFF and ON conditions in 2 groups of Parkinson’s disease patients with or without neuropathic pain. We also compared pain-induced cerebral activations during experimental nociceptive stimulations using H215O positron emission tomography in both deep brain stimulation OFF and ON conditions. Correlation analyses were performed between clinical and neuroimaging results. Deep brain stimulation significantly increased subjective heat pain threshold (from 40.3 ± 4.2 to 41.6 ± 4.3, P = .03) and reduced pain-induced cerebral activity in the somatosensory cortex (BA 40) in patients with pain, whereas it had no effect in pain-free patients. There was a significant negative correlation in the deep brain stimulation OFF condition between pain threshold and pain-induced activity in the insula of patients who were pain free but not in those who had pain. There was a significant positive correlation between deep brain stimulation-induced changes in pain threshold and in pain-induced cerebral activations in the primary somatosensory cortex and insula of painful patients only. These results suggest that subthalamic nuclei deep brain stimulation raised pain thresholds in Parkinson’s disease patients with pain and restored better functioning of the lateral discriminative pain system.
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aINSERM, Imagerie cérébrale et handicaps neurologiques, Toulouse, France
bUniversité de Toulouse, Imagerie cérébrale et handicaps neurologiques, Toulouse, France
cDepartment of Neurology, University Hospital of Toulouse, Toulouse, France
dINSERM, Clinical Investigation Center, Purpan, Toulouse, France
eDepartment of Neurosurgery, University Hospital of Toulouse, Toulouse, France
fDepartment of Clinical Pharmacology, University of Medicine, Toulouse, France
*Corresponding author. Address: INSERM U825, Pavillon Baudot, CHU Purpan, 31059 Toulouse, France. Tel.: +33 05 81 18 49 84.
Article history: Received 10 February 2012; Received in revised form 18 July 2012; Accepted 24 July 2012.