Influence of Dopaminergic Medication on Conditioned Pain Modulation in Parkinson's Disease Patients.
BACKGROUND
Pain is highly prevalent in patients with Parkinson's disease (PD), but little is known about the underlying pathophysiological mechanisms. The susceptibility to pain is known to depend on ascending and descending pathways. Because parts of the descending pain inhibitory system involve dopaminergic pathways, dysregulations in dopaminergic transmission might contribute to altered pain processing in PD. Deficits in endogenous pain inhibition can be assessed using conditioned pain modulation (CPM) paradigms.


METHODS
Applying such a paradigm, we investigated i) whether CPM responses differ between PD patients and healthy controls, ii) whether they are influenced by dopaminergic medication and iii) whether there are effects of disease-specific factors. 25 patients with idiopathic PD and 30 healthy age- and gender-matched controls underwent an established CPM paradigm combining heat pain test stimuli at the forearm and the cold pressor task on the contralateral foot as the conditioning stimulus. PD patients were tested under dopaminergic medication and after at least 12 hours of medication withdrawal.


RESULTS
No significant differences between CPM responses of PD patients and healthy controls or between PD patients "on" and "off" medication were found. These findings suggest (i) that CPM is insensitive to dopaminergic modulations and (ii) that PD is not related to general deficits in descending pain inhibition beyond the known age-related decline. However, at a trend level, we found differences between PD subtypes (akinetic-rigid, tremor-dominant, mixed) with the strongest impairment of pain inhibition in the akinetic-rigid subtype.


CONCLUSIONS
There were no significant differences between CPM responses of patients compared to healthy controls or between patients "on" and "off" medication. Differences between PD subtypes at a trend level point towards different pathophysiological mechanisms underlying the three PD subtypes which warrant further investigation and potentially differential therapeutic strategies in the future.
Department of Neurology, University Medical Center Hamburg Eppendorf, Hamburg, Germany.
Wiebke
W
Grashorn
Department of Neurology, University Medical Center Hamburg Eppendorf, Hamburg, Germany.
Odette
O
Schunke
Department of Neurology, University Medical Center Hamburg Eppendorf, Hamburg, Germany.
Carsten
C
Buhmann
Clinic for Neurology at the Medical Faculty, University of Duisburg-Essen, Essen, Germany.
Katarina
K
Forkmann
Department of Neurology, University Medical Center Hamburg Eppendorf, Hamburg, Germany.
Sabrina
S
Diedrich
Department of Neurology, University Medical Center Hamburg Eppendorf, Hamburg, Germany.
Katharina
K
Wesemann
Clinic for Neurology at the Medical Faculty, University of Duisburg-Essen, Essen, Germany.
Ulrike
U
Bingel
D000368:Aged; D000369:Aged, 80 and over; D003213:Conditioning, Psychological / Q000187:drug effects / Q000502:physiology; D015259:Dopamine Agents / Q000494:pharmacology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010147:Pain Measurement / Q000379:methods; D058748:Pain Perception / Q000187:drug effects*; D017288:Pain Threshold / Q000187:drug effects* / Q000502:physiology; D010300:Parkinson Disease / Q000503:physiopathology*
D015259:Dopamine Agents