Pain sensitivity and descending inhibition of pain in Parkinson's disease

Publication

Pain sensitivity and descending inhibition of pain in Parkinson's disease

Journal Paper/Review - Jul 24, 2008

Mylius Veit, Engau I, Teepker M, Stiasny-Kolster K, Schepelmann K, Oertel W H, Lautenbacher S, Möller J C

PubMed

18653553

Doi

10.1136/jnnp.2008.145995

Citation

Mylius V, Engau I, Teepker M, Stiasny-Kolster K, Schepelmann K, Oertel W, Lautenbacher S, Möller J. Pain sensitivity and descending inhibition of pain in Parkinson's disease. J Neurol Neurosurg Psychiatry 2008; 80:24-8.

Type

Journal Paper/Review (English)

Journal

J Neurol Neurosurg Psychiatry 2008; 80

Publication Date

Jul 24, 2008

Issn Electronic

1468-330X

Pages

24-8

Brief description/objective

BACKGROUND
Patients suffering from Parkinson's disease (PD) often complain about painful sensations. Recent studies detected increased subjective pain sensitivity and increased spinal nociception, which appeared to be reversible by dopaminergic treatment. Possibly, reduced descending pain inhibition contributes to this finding.

OBJECTIVE
Subjective pain thresholds as well as nociceptive reflex thresholds were investigated to isolate potential loci of the pathophysiological changes within the pain pathway. In addition, the diffuse noxious inhibitory control (DNIC) system as one form of descending control was assessed.

METHOD
15 patients with PD and 18 controls participated in the study. Electrical and heat pain thresholds as well as the nociceptive flexion reflex (NFR) thresholds were determined. Thereafter, the electrical pain thresholds were measured once during painful heat stimulation (conditioning stimulation) and twice during innocuous stimulation (control stimulation).

RESULTS
Patients with PD exhibited lower electrical and heat pain thresholds as well as lower NFR thresholds. Suppression of the electrical pain thresholds during painful heat stimulation (conditioning stimulation) compared with control stimulation did not differ significantly between the groups. No differences in the thresholds between patients with PD with and without clinical pain were seen.

CONCLUSIONS
Finding the NFR threshold to be decreased in addition to the decreased electrical and heat pain thresholds indicates that the pathophysiological changes either already reside at or reach down to the spinal level. Reduced activation of the DNIC system was apparently not associated with increased pain sensitivity, suggesting that DNIC-like mechanisms do not significantly contribute to clinical pain in PD.