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J Neurol Neurosurg Psychiatry 80:24-28 doi:10.1136/jnnp.2008.145995
  • Research paper

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

  1. V Mylius1,
  2. I Engau1,
  3. M Teepker1,
  4. K Stiasny-Kolster1,
  5. K Schepelmann3,
  6. W H Oertel1,
  7. S Lautenbacher2,
  8. J C Möller1
  1. 1
    Department of Neurology, Philipps University of Marburg, Germany
  2. 2
    Physiological Psychology, Otto-Friedrich-University of Bamberg, Germany
  3. 3
    Schlei-Klinikum Schleswig MLK, Schleswig, Germany
  1. Dr V Mylius, Department of Neurology, Philipps University of Marburg, Rudolf-Bultmann-Str 8, 35033 Marburg, Germany; mylius{at}med.uni-marburg.de
  • Received 30 January 2008
  • Revised 19 June 2008
  • Accepted 30 June 2008
  • Published Online First 24 July 2008

Abstract

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.

Footnotes

  • Competing interests: None.

  • Ethics approval: The study was approved by the ethics committee of the University of Marburg, Germany.

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