Pain appears to be more common in individuals with Parkinson’s disease than in those without, suggesting that pain is associated with the condition, according to a report in the September issue of Archives of Neurology, one of the JAMA/Archives journals.
“Patients with Parkinson’s disease often complain of painful sensations that may involve body parts affected and unaffected by dystonia,” or involuntary muscle contractions, the authors write as background information in the article. This pain may resemble cramping or arthritis, or have features of pain caused by nerve damage. “The high frequency of these pain disorders in the general population makes it hard to establish whether pain is more frequent among people with Parkinson’s disease than among age-matched controls.”
Giovanni Defazio, M.D., Ph.D., of the University of Bari, Italy, and colleagues compared 402 patients with Parkinson’s disease to 317 healthy individuals who were the same age. Participants provided information about their current age, the age at which they developed Parkinson’s disease, scores on disease rating scales and details regarding any pain that was present at the time of the study and lasted for at least three months.
Overall, pain was more common among Parkinson’s disease patients than among controls (281 or 69.9 percent vs. 199 or 62.8 percent). This was mainly attributable to dystonic pain, as rates of pain not associated with dystonia were similar among individuals with Parkinson’s disease (267 or 66.4 percent) and those without (199 or 62.8 percent).
“Nevertheless, we observed a significant association between Parkinson’s disease and non-dystonic pain, beginning after the onset of parkinsonian symptoms,” the authors write. “Cramping and central neuropathic [nervous system–related] pain were more frequent among Parkinson’s disease patients than controls. About one-quarter of patients who experienced pain reported pain onset before starting antiparkinsonian therapy.”
Basal ganglia, structures deep in the brain that control movement and are damaged in patients with Parkinson’s disease, also are involved with pain processing, the authors note. This might account for the increase in pain associated with Parkinson’s disease.
“These data support the hypothesis that pain begins at clinical onset of Parkinson’s disease or thereafter as a non-motor feature of Parkinson’s disease,” they conclude. “The findings of this study may have implications for designing studies aimed at understanding pain mechanisms in Parkinson’s disease and identifying specific treatment strategies.”
Arch Neurol. 2008;65:1191-1194.