Subjective pain perception, spinal nociception and descending inhibition of experimentally induced pain in Parkinson's disease

Patients suffering from Parkinson's disease (PD) complain more often about acute and chronic pain, which can be subdivided into musculoskeletal pain, radicular-neuropathic pain, dystonic pain, central pain and akathisia. Previous studies of experimentally induced pain in PD revealed heterogeneous results. One recent study detected an increased perception of heat-induced pain, which was reversible after dopaminergic treatment. Possibly a reduced dopaminergic descending inhibitory control (DNIC) system contributes to this finding. Therefore, we investigated the DNIC system by using a tonic heat stimulus and a phasic electrical stimulus. In addition to thermal and electrical pain thresholds, we assessed spinal nociception by using the nociceptive flexion reflex (NFR).

Ten patients with PD (Hoehn and Yahr Stage I-III) and fifteen age-matched controls participated in the study, which was performed in the morning without any medication. The sural nerve on the more affected side was stimulated electrically. Thermal stimulation was done by using a thermode on the contra lateral forearm. The NFR motor response was recorded from the biceps femoris muscle. Following a neurological and neuropsychological examination, thermal heat and electrical pain thresholds as well as the NFR thresholds were determined by using the staircase method. Thereafter, pain thresholds and the supra-threshold NFR response with corresponding verbal pain ratings were measured during DNIC and control condition.

The PD patients showed significantly lower NFR thresholds (9.8±9.6 mA vs.16.7±6.3 mA, p<0.01), while the thermal and electrical pain thresholds were not changed significantly. The suppression of spinal pain responses and verbal pain ratings during DNIC condition compared to control condition did not differ significantly between the groups.

Finding the NFR threshold to be markedly decreased in PD indicates an increased nociception on the spinal level. However, a reduced dopaminergic descending inhibition could not be detected by the investigation of the DNIC system, suggesting that other spinal or supra spinal systems are involved. We conclude that nociception is enhanced in PD presumably leading to an increase of clinical pain.