Electrophysiological assessment of nociception in patients with Parkinson's disease: A multi-methods approach.

J Neurol Sci 2016 Sep 28;368:59-69. Epub 2016 Jun 28.

University of Bamberg, Department of Physiological Psychology, Bamberg, Germany.

Objective: Nociceptive abnormalities indicating increased pain sensitivity have been reported in patients with Parkinson's disease (PD). The disturbances are mostly responsive to dopaminergic (DA) treatment; yet, there are conflicting results. The objective of the present study was to investigate pain processing and nociception in PD patients in a more comprehensive manner than previous studies. For this purpose, a multi-methods approach was used in order to monitor different levels of the central nervous system (spinal, subcortical-vegetative, cortical).

Methods: The heat-pain threshold, contact-heat evoked brain potentials (CHEPs) and sympathetic skin responses (SSR), nociceptive flexion responses (NFR) and subjective pain ratings were measured in 23 idiopathic PD patients both in the Off-phase (without DA medication) and On-phase (after DA medication intake) as well as in 23 healthy controls.

Results: Compared to controls, PD patients showed decreased heat-pain thresholds only in the Off and tentatively increased NFR amplitudes in both phases. We found no between-group differences for the CHEPs, the NFR threshold/latency or the pain ratings. Yet, SSR amplitudes/frequencies were decreased and latencies were increased in PD patients in both phases. Correlations between CHEPs amplitudes and pain ratings were found only in controls.

Discussion: Increased pain sensitivity (heat-pain threshold) in the Off which normalizes in the On argues for DA induced dysfunctions of the nigrostriatal pain loops with the basal ganglia as main circuit in our PD sample. Dysfunctions of the subcortical-vegetative parameters despite of inconspicuous cortical nociception suggest disturbances of the central or peripheral innervation of sympathetic branches with coincidently intact ascending pathways in the PD group.

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http://dx.doi.org/10.1016/j.jns.2016.06.058DOI Listing
September 2016
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